PPARδ in T Cells and Colorectal Cancer Immunotherapy

ContributorsProf. Dr. Mustafa ÖzdoğanAuthor · Medical review · Editorial approval

PublishedOct 19, 2026

25 min read

PPARδ in T Cells and Colorectal Cancer Immunotherapy

In this article

One Protein, Two Cells: Why PPARδ Fuels Tumors in Cancer but Curbs Them in Immune Cells

Most colon and rectal cancers are microsatellite stable (MSS) and do not respond to today's immunotherapies. A study published in Nature Immunology on October 14, 2026 shows that PPARδ, a protein that controls how cells burn fatty acids, has opposite effects depending on the cell in which it is activated: in cancer cells it increases tumor growth, while in immune cells (especially CD8+ T cells) it suppresses tumors. In mouse models, T cells with increased PPARδ activity strengthened tumor rejection and metastasis control in resistant MSS tumors when combined with anti-PD-1 immunotherapy, and the tumor-destroying capacity of human CAR-T cells also increased. All of this is mouse, organoid and cell-culture data; no patient has been treated with this approach.

Quick Answer · Physician Summary

What was found: When PPARδ was activated in cancer cells, tumor growth increased and the immune response weakened; when it was activated in immune cells, tumors were suppressed in mouse models, and this effect overrode the negative effect of activation in the cancer cells. CD8+ T cells were found to be both necessary and sufficient for this effect.
Together with anti-PD-1: In a resistant MSS colorectal cancer model, the tumor was completely rejected in 6 of 12 mice (50%) that received PPARδ-activated CD8+ T cells plus anti-PD-1 treatment, compared with 1 of 10 (10%) among those that received normal T cells. Metastasis rates were 15.4% versus 72.7%.
Caution: The data come from mice, organoids and cell culture, and PPARδ was mostly switched on genetically. Because tumors can grow when PPARδ is also switched on in cancer cells, activating it with a drug in every cell may backfire.
In practice: There is no treatment applicable to patients and no human data yet. Substances that activate PPARδ (for example GW501516, "cardarine") should not be used as drugs or supplements.

Why does this topic matter?

Cancers that are rising at younger ages include colorectal cancer. The paper notes that in the United States, cancer-related loss of life under age 50 is the leading cause among men and the second among women. Most tumors are MSS and mismatch repair proficient (pMMR). These tumors resist both immune checkpoint inhibitors (ICB) and CAR-T cell therapy; the response to current treatments is especially poor in metastatic MSS colorectal cancer.

In contrast, immunotherapy can benefit tumors with a deficient DNA repair system (MMR-deficient, MSI-high); the immunotherapy approvals in MMR-deficient colon cancer are one example. The anti-PD-1 drugs pembrolizumab and nivolumab and the anti-CTLA-4 drug ipilimumab release the brakes on immune cells. As the paper emphasizes, the problem is not only releasing the brakes; the immune cell also needs the resilience to function inside a tumor that evades immunity. Alongside regimens used in MSS tumors today, such as FOLFOX and FOLFIRI with bevacizumab, this study aims to strengthen the immune cell itself.

A tumor works like an ecosystem in which cancer cells and immune cells share the same nutrients and energy sources. The authors argue that tumor progression may reflect not only uncontrolled growth of the cancer cell but also the failure of the immune cell to maintain its "fitness" in this competition. PPARδ is a gene-regulating protein that senses lipids and controls fatty acid burning (fatty acid oxidation, FAO); it is present in both cancer and immune cells. Earlier studies were contradictory: some reported that its activation in cancer cells increased tumor formation, others that its loss increased polyp burden in mice and that ligand activation could reduce carcinogenesis. In T cells, too, PPARδ has been found to be both supportive and suppressive. The question of this study is therefore clear: does the effect of PPARδ depend on the cell in which it is activated?

Is this the first time PPARδ has been shown to suppress tumors in immune cells?

No. The topic has been debated for years with conflicting results; the contribution of this study is that it genetically activated the two cell groups separately in the same models and compared them. Precedents from the paper's reference list:

2004–2006: PPARδ was reported to suppress colon carcinogenesis (Harman et al., 2004), and ligand activation was reported to inhibit colon carcinogenesis (Marin et al., 2006).
2014–2019: In contrast, PPARδ/β overexpression in the colonic epithelium was reported to increase colon cancer susceptibility (Zuo et al., 2014), and PPARD to accelerate colorectal tumor formation, progression and invasion (Liu et al., 2019).
2016: A high-fat diet was shown to increase the PPARδ program in intestinal stem cells and facilitate tumor formation (Beyaz et al., Nature; the same laboratory). See the site's article on nutrition and cancer.
2018–2019: PPAR agonists were reported to increase fatty acid burning in T cells, expand tumor-specific CD8+ T cells and support the effect of anti-PD-1 and cell therapy (Chowdhury et al.; Saibil et al.).
2024: PPARβ/δ was reported to support memory CD8+ T cell formation (Bevilacqua et al.), while another study (Cen et al.) proposed that PPARδ suppresses CD8+ T cell cytotoxicity.
2026: This study showed that activation in immune cells overrides activation in cancer cells, in MSS and metastatic models and in human CAR-T cells.

What is PPARδ, and what happens when it is activated in an immune cell?

PPARδ is a gene-regulating protein that controls how cells burn fatty acids. Activated in a cancer cell, it increases tumor growth; activated in an immune cell, especially a CD8+ T cell, it strengthens tumor control in mouse models. Results come from mice, organoids and cell culture; patient treatment has not been tested.

How was the study done?

The study was led by Semir Beyaz at Cold Spring Harbor Laboratory; Paul Bunk, Ilgin Ergin, Timothy Maher and Vyom Shah are listed as co-first authors with equal contribution. The researchers switched PPARδ on largely genetically, not with a drug: by fusing an activator region called VP16/VP64 to PPARδ, the protein was made constitutively active without needing a binding molecule (ligand) (gain of function, GOF). This made it possible to compare outcomes in the same tumor model when PPARδ was switched on only in cancer cells (cGOF), only in immune cells (iGOF, in all blood-derived immune cells), or in both.

Model	What was done?	What was found?
Mouse, subcutaneous MC38 (MSI-like, highly mutated colon cancer)	PPARδ switched on only in cancer, only in immune cells, or in both	Growth increased when switched on in cancer; tumors shrank when switched on in immune cells
Mouse, AKP and AKPS organoids placed in the colon (MSS, immune-evasive)	Activation in immune cells; spleen cell transfer	Tumor growth and metastasis were restricted
Mouse, B16-F10 melanoma and EO771 breast tumor	Activation in immune cells	Tumor growth decreased
Mouse, activation only in CD8+ T cells and cell transfer	Tamoxifen-induced CD8+ T activation; transfer of PPARδ-active T cells	Tumor control and CD8+ T cell entry into the tumor increased
Human, patient-derived organoids and the person's own blood cells (1 MSS, 1 MSI)	Blood cells were pretreated with GW501516	Cytotoxicity against the organoids increased
Human CAR-T cells (EGFR- and HER2-targeted)	GW501516 or genetic PPARδ activation	Destruction of tumor cells increased; HER2 CAR-T reduced tumor growth in mice bearing ovarian cancer cells

Findings: the result depends on the cell in which PPARδ is switched on

1. Activation in the immune cell overrode activation in the cancer cell

In MC38 tumors, switching PPARδ on only in the cancer cell increased tumor growth, consistent with earlier reports (P = 0.002). In mice with PPARδ switched on in immune cells, however, both normal and PPARδ-active cancer cell tumors remained significantly smaller (P < 0.0001).

Single-cell RNA and chromatin sequencing supported this picture. Activation in the cancer cell increased genes linked to survival, proliferation and immune suppression. In the T cells of these tumors, expression and chromatin accessibility rose in genes linked to exhaustion (dysfunction) (Ctla4, Pdcd1, that is PD-1, Havcr2, Lag3). When PPARδ was also on in immune cells, these genes decreased, and genes linked to apoptosis and immune recognition increased in the cancer cells. The authors interpret this as activation on the immune side turning the tumor microenvironment from a suppressive state into one that stimulates immunity.

Figure 1 · One protein, two cells, opposite results

A simplified framework based on mouse models; not a firm rule.

How to read it: The top box states that the effect of PPARδ depends on the cell in which it is activated. The left box shows that activation in the cancer cell increases tumor growth and weakens the immune response; the green box on the right shows that activation in the immune cell restricts tumor growth and increases T cell entry. The middle box states that when activation is present in both cells in the mouse MC38 model, the immune side's effect prevailed. The dashed bottom box indicates that treatment of patients with a PPARδ activator has not been tested.

2. Tumors were restricted in MSS and metastatic models too

Immune-evasive MSS organoid models placed in the colon were used (AKP, and the more aggressive AKPS, which spontaneously metastasizes to the liver and other organs). Tumor growth was restricted in mice with PPARδ active in immune cells. When spleen cells (splenocytes) from PPARδ-active mice were given to irradiated normal mice, AKPS tumor mass decreased (P = 0.0022) and the metastasis rate fell from 44.4% (4/9) to 0% (0/4); however, this rests on a small group of 4 animals.

AKPS metastasis rate after transfer of immune cells

Percent. The colored bar shows mice that received PPARδ-active (iGOF) mouse splenocytes; the gray bar shows mice that received normal (WT) splenocytes.

PPARδ-active splenocytes (0/4)

Normal splenocytes (4/9)

44.4%

Two arms of the same experiment (n = 4 and n = 9). The absolute difference is about 44 points; because it rests on very small numbers, it should not be read as a precise effect size. Tumor mass also decreased in the same experiment (P = 0.0022).

Similar tumor restriction was seen in melanoma (B16-F10) and breast cancer (EO771) models. At the tissue level, immune cell density around the tumor and cell networks called "immune hubs" increased; AKP tumors were less fibrotic. The increase in the number of CD45+ immune cells in MC38 tumors was marked (P = 1.25 × 10⁻⁹), but this analysis rested on 6 areas taken from two mice in each group. In mice in which PPARδ was deleted in immune cells, MC38 tumor growth did not change significantly; the authors attribute this most likely to compensation by other PPAR family members.

3. CD8+ T cells are necessary and sufficient for this effect

When CD8+ T cells were depleted in PPARδ-active mice, tumor growth accelerated. Switching PPARδ on only in CD8+ T cells (with a tamoxifen-inducible system) reduced tumor growth; it increased the number of CD8+ T cells entering the tumor and the proportion of "polyfunctional" cells producing both IFNγ and TNF. Transferring CD8+ T cells from PPARδ-active mice into normal mice also suppressed tumor growth. These cells carried more CXCR3, the receptor for the chemokines (CXCL9/CXCL10) that guide cells to the tumor; depleting CXCR3+ cells increased tumor growth in PPARδ-active mice. In a dataset of human melanoma tumor cells, a moderate positive correlation was found between the PPAR activity score and IFNG and CXCR3 expression (R = 0.37 and 0.45); correlation does not show causation.

4. Mechanism: opening of chromatin and fat burning (Cpt1a)

PPARδ activation made chromatin more accessible around genes linked to effector function in CD8+ T cells (for example Prf1, Gzmb, Ccl4, Klrg1); binding motifs of AP-1 transcription factors were enriched in these regions. AP-1 is a group of factors linked to T cell effector function, resistance to exhaustion and CAR-T efficacy.

On the metabolic side, carnitine levels fell in PPARδ-active T cells, while expression of Cpt1a (the enzyme that starts the entry of fatty acids into mitochondria) and palmitate oxidation increased. Deleting Cpt1a in immune cells partly blunted the effect of PPARδ. Conversely, a Cpt1a mutant that is not suppressed by malonyl-CoA increased fat burning and memory-like features but did not, on its own, significantly suppress tumor growth. So Cpt1a-mediated fat burning is necessary for this effect but not sufficient on its own. The depletion of most fatty acid species (such as palmitic, palmitoleic and oleic acid) in the tumors of PPARδ-active mice is consistent with immune cells competing with cancer for nutrients; however, this competition was not shown directly with isotope tracing.

5. Together with anti-PD-1: tumor rejection in a resistant MSS model

Anti-PD-1 therapy remains weak in MSS tumors. The researchers therefore transferred normal or PPARδ-active CD8+ T cells into irradiated mice carrying established AKPS tumors and then gave anti-PD-1 (Figure 2).

Figure 2 · Design of the CD8+ T cell transfer experiment with anti-PD-1

Simplified timeline; mouse experiment.

How to read it: First, immune-evasive AKPS organoids are injected into the colon of the mice. On day 9, both groups receive the same whole-body irradiation. Two days later, 3 million CD8+ T cells from normal or PPARδ-iGOF mice are given by vein. After the T cells have settled in, 9–11 days later, anti-PD-1 treatment is given every 2–3 days for 14 days. The measured outcomes are tumor rejection, metastasis and tumor weight; survival did not differ significantly when anti-PD-1 was given alone. In a separate experiment in which anti-PD-1 and anti-CTLA-4 were given together, a survival benefit was seen.

In mice that received normal T cells, tumors continued to grow and metastasize; in mice that received PPARδ-active T cells, tumor growth and metastasis decreased significantly, and the tumor was completely rejected in half of them.

Tumor rejection and metastasis in mice given CD8+ T cells together with anti-PD-1

Percent. The colored bar shows mice that received PPARδ-active (iGOF) CD8+ T cells; the gray bar shows mice that received normal (WT) CD8+ T cells. Resistant MSS (AKPS) colorectal cancer model.

Tumor rejection, day 35 · PPARδ-active T (6/12)

50%

Tumor rejection, day 35 · normal T (1/10)

10%

Metastasis · PPARδ-active T (2/13)

15.4%

Metastasis · normal T (8/11)

72.7%

Two arms of the same experiment. The metastasis difference reported in the paper is significant (z test for proportions, P = 0.0005). Absolute difference: 40 points for tumor rejection and about 57 points for metastasis. Each percentage rests on 10–13 animals; animal numbers are small. Recipient mice were irradiated before the T cells were given.

In absolute numbers: tumor rejection 6/12 (50%) versus 1/10 (10%); metastasis 2/13 (15.4%) versus 8/11 (72.7%), that is, about one fifth. Tumor weight also fell (P = 0.0094). However, this gain did not carry over to survival: given alone, anti-PD-1 did not significantly improve overall survival. When anti-PD-1 and anti-CTLA-4 were given together, survival was better in mice that received PPARδ-active T cells (P = 0.0121; 14 mice with normal T cells, 15 with PPARδ-active T cells). Irradiation may have contributed; however, the two groups were treated identically.

6. Human cells: organoids and CAR-T

Two patient-derived organoid lines (one MSS, one MSI) were used. Each organoid was co-cultured with the same person's own blood cells (PBMC); when the blood cells were pretreated with the PPARδ agonist GW501516, cytotoxicity (caspase-3/7 signal) against both organoids rose significantly (P = 0.0003 and P = 0.0002). When EGFR-targeted CAR-T cells were pretreated with GW501516, organoid destruction also rose (P = 0.0033 for MSI, P < 0.0001 for MSS); there was no difference with untreated "mock" T cells.

In HER2-targeted CAR-T cells, PPARδ was activated genetically. In the laboratory these cells destroyed more cancer cells carrying HER2; fatty acid burning, effector genes and chromatin accessibility increased, and exhaustion-linked genes (BTLA, TOX2) decreased. In immunodeficient (NSG) mice, PPARδ-active CAR-T cells reduced the growth of established SK-OV-3 tumors more (P = 0.0161; 13 mice per group).

There is an important detail here: press releases describe the CAR-T experiments in a colorectal cancer frame. In the paper, however, the colorectal organoid experiment was done with EGFR-targeted CAR-T cells pretreated with GW501516; the mouse experiment used ovarian cancer cells. The safety of the CAR-T cells (for example cytokine release syndrome) was not assessed in this study. Research on CAR-T in solid tumors continues; this finding suggests a metabolic add-on strategy for that field.

Safety: no excessive inflammation, but follow-up was short

In PPARδ-active mice, immune cells in the spleen did not increase inflammatory genes; no autoimmunity or abnormal immune activity was seen in the lung, spleen, heart, kidney, liver, small intestine or colon. Lifespan and body weight were similar to controls, and disease severity in experimental colitis was also similar. The authors state that these results support therapeutic potential but that longer-term safety studies are essential. In patients, the known side effects of immunotherapy remain a real clinical concern.

Why is turning this into a human treatment not easy?

First, because PPARδ can also promote tumors in the cancer cell, switching it on with a drug in every cell could backfire; the paper stresses that these context-dependent differences must be well understood in order to design treatments that minimize possible pro-cancer effects while maximizing the immune effect. Second, PPARδ in the study was mostly switched on with a ligand-independent genetic activator; this does not mimic all functions of native PPARδ. Third, most animal experiments were short and used small groups.

How is the conflict with earlier studies explained?

Feature	Cen et al. (2024)	This study (2026)
Intervention on PPARδ	Whole-body deletion of PPARδ, overexpression of native PPARδ, continuous GW501516 in cell culture	Ligand-independent activation with VP16/VP64 in immune, CD8+ T and CAR-T cells; plus prolonged GW501516 pretreatment
Main result	PPARδ suppressed CD8+ T cytotoxicity by blocking RelA (NF-κB) DNA binding	Activation in CD8+ T cells increased cytotoxicity and tumor control
Authors' explanation	—	The difference may stem from activation state, cellular compartment, context and timing; RelA/NF-κB repression was not measured in this study

Level of evidence: what was shown, what was not?

Topic	Status
Mouse colorectal, melanoma and breast tumor models	ShownWith genetic activation; only 4–15 animals in some groups
Tumor rejection and metastasis control with anti-PD-1	PartlySurvival difference not significant with anti-PD-1 alone; survival benefit with anti-CTLA-4 added
Effect in human cells	PartlyTwo patient-derived organoid lines; for CAR-T, laboratory plus a single mouse model (ovarian)
Selective drug delivery to immune cells	Not shownNo selective activation method in this study
Effect and safety in patients	Not shownNot tested in humans; long-term safety unknown

Warning: this study is not a reason to take PPARδ supplements

GW501516 (also sold as cardarine and endurobol), used in the cell experiments, is not approved as a drug in any country. Its development was abandoned in 2007 after animal studies showed cancers in several organs; it is on the World Anti-Doping Agency (WADA) prohibited list and is often mislabeled online as a "SARM". In the study by Cen and colleagues, GW501516 increased intestinal adenoma burden in mice. Because the same pathway can also increase tumor growth in the cancer cell, it cannot be concluded that using a PPARδ-activating substance would benefit a person. For details, see the article on athlete supplements and cancer risk.

The situation in Turkey

The approach tested in this study (selectively activating PPARδ in immune cells) is not a drug or patient treatment; it is a finding at the level of mice, organoids and cell culture. The paper does not report any PPARδ-activating treatment tested in humans, and press releases also state that the approach is not yet proven in patients. Options such as a license (TİTCK, the Turkish Medicines and Medical Devices Agency), reimbursement (SGK/SUT, the Social Security Institution and its drug payment schedule), import of a drug from abroad or off-label use therefore do not apply to this approach. Because the TİTCK license query and clinical trial registries were not searched for this article, it could not be verified whether any clinical trial of this approach is running in Turkey or abroad. The research tool GW501516 is not approved as a drug. For the payment conditions of current checkpoint inhibitors, see the articles on immunotherapy reimbursement conditions and the SUT guide; their status in MSS colorectal cancer could not be verified for this article.

Practical advice for patients and their families

This study does not describe a treatment that can be used today. Discuss the options that apply to your own disease with your oncologist.
In colorectal cancer, the tumor's MMR/MSI status is important for the immunotherapy decision. Make sure this result appears in your biopsy report; if needed, ask about molecular tests such as next-generation sequencing.
Do not use substances or supplements claimed to activate PPARδ (GW501516, "cardarine", "endurobol"). During cancer treatment, do not take supplements without consulting your oncologist.
New approaches first go through preclinical and clinical stages; for suitable patients, clinical trials may be an option.
Colorectal cancer is also rising at younger ages. Read about the new screening age guideline and screening with colonoscopy.

Frequently asked questions

What is PPARδ, and why does it have opposite effects in cancer?: PPARδ is a gene-regulating protein that controls how cells burn fatty acids. When it is activated in a cancer cell, tumor growth increases; when it is activated in an immune cell, especially a CD8+ T cell, tumor control becomes stronger in mouse models. The authors explain this difference by an effect that varies with cell type and context.
After this study, can drugs or supplements that activate PPARδ be used?: No. The activation in the study was mostly genetic and specific to immune cells; substances such as GW501516 are not approved as drugs and have been linked to cancer risk in animal studies. Because the same pathway can increase tumor growth in the cancer cell, using them on their own may cause harm.
Why does MSS colorectal cancer not respond to immunotherapy, and what did this study change?: In MSS tumors, immune cell entry, persistence and function are limited. In a mouse model, the study showed that PPARδ-active CD8+ T cells entered the tumor more and functioned better, producing tumor rejection and less metastasis with anti-PD-1. The effect in humans is unknown.
When could this approach be tried in patients?: There is no timeline. A method for selective activation in immune cells (cell engineering or targeted delivery) and long-term safety data are needed first. The first step in humans would be a phase 1 trial, after sufficient safety data.

Glossary

PPARδ: A transcription factor (gene-regulating protein) that senses lipids and regulates genes linked to fatty acid burning.
Fatty acid oxidation (FAO): The cell burning fatty acids in mitochondria to obtain energy.
Cpt1a: The enzyme that starts the entry of fatty acids into mitochondria.
MSS / MSI: Microsatellite stable / microsatellite unstable. MSI tumors have a deficient DNA repair system (MMR) and are more likely to respond to immunotherapy.
CD8+ T cell: An immune cell that can recognize and destroy cancer cells.
Organoid: A miniature tissue grown in the laboratory from a patient's tumor that carries the tumor's genetic makeup.
CAR-T cell: A T cell genetically modified to recognize a cancer target.
Immune checkpoint inhibitor (ICB): Drugs such as anti-PD-1 and anti-CTLA-4 that release the brakes on immune cells.

DROZDOGAN Academy Commentary

This study is a clear example that the same pathway can give opposite results depending on the cell in which it works, and that "on or off" logic cannot be applied without considering cell type.

⚡ Why it matters

MSS colorectal cancer is the disease that benefits least from immunotherapy and is rising at younger ages. The study looks for the solution not only in releasing the brakes but in increasing the resilience of the immune cell inside the tumor, and for this it points to a metabolic target (fat burning) together with a chromatin program.

✅ Strengths

Multiple models (MSI, MSS, metastatic, melanoma, breast), both activation and deletion experiments, necessity and sufficiency tests in CD8+ T cells, Cpt1a loss and gain models, human organoids and CAR-T cells. The authors openly discuss the conflicting literature and their own limits.

⚠️ Limitations

Genetic, constitutive activation is not the same as activation with a drug. In many experiments the number of animals is small, and some statistics rest on tumor areas or cell counts rather than mice. The transfer experiments involve irradiation, and anti-PD-1 alone did not significantly improve survival. Human data are limited to two organoid lines; the CAR-T mouse experiment was done in an ovarian model in immunodeficient mice. The authors disclosed a patent application.

🩺 In practice

There is no recommendation for patients. The tumor's MMR/MSI status should be known, and current standard treatments should be given on the decision of the oncologist and the tumor board. No PPARδ-activating substance or supplement should be used.

❓ Open questions

How will selective activation in immune cells be achieved: cell engineering or targeted delivery? What will long-term safety look like? Is the effect also seen in the patient's own T cells in MSS disease? Which mechanisms besides Cpt1a are required? For CAR-T, is the best approach genetic activation or drug pretreatment?

Conclusion: The effect of PPARδ varies with the cell it is in; when switched on in immune cells, it produces a strong effect against MSS colorectal tumors in mouse models. This is a promising laboratory finding; selective delivery and human safety have not yet been shown for it to become a patient treatment.

Transparency note

This article was prepared in October 2026.
The data were taken from the full text and figure legends of the article published online in Nature Immunology on October 14, 2026 (accepted September 9, 2026, open access). The journal volume and page information could not be verified while this article was prepared. The Cold Spring Harbor Laboratory press release and news summaries were used for comparison; where statements differed, the paper was taken as the basis.
Information on earlier studies was taken from the paper's reference list; the adenoma finding of Cen and colleagues' study was taken from its published abstract. Information on GW501516 is based on statements by anti-doping and health authorities.
The license, SGK/SUT status and clinical trial registries in Turkey were not searched for this article and therefore could not be verified.
The P = 0.0005 value reported in Figure 7e of the paper does not match the proportion test calculated from the numbers shown in the panel, 8/11 and 2/13 (about 0.005); the figure legend also says n = 12 for the comparison group, while the panel shows 11. The paper's values were transferred as they are; the difference remains significant in either case.
It was verified from the paper that Ilgin Ergin is a co-first author; nationality information circulating in the press and on social media could not be verified from the paper, so it was not included in the article.
The authors reported a patent application on activating metabolic switches in immune cells (63/460,971) and company and CAR-T-related patent ties for some authors.
The comparisons in the charts each belong to randomized arms of the same experiment; no comparison across different studies was made. The diagram is derived from the text and contains no new data. The academy commentary is our own.

Sources

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