What makes Tat-MYC unique​

1. Receptor-independent: Enters cells directly, bypassing surface receptor limitations.​
2. Direct nuclear action: Restores the suppressed mTOR–MYC axis, reigniting metabolic and transcriptional programs essential for T cell function.​
3. Downstream of IL-2, but safer: Mimics IL-2’s growth and cytotoxicity benefits without cytokine storm risks.​
4. Transient & controlled: Naturally degrades in 3–5 days, ensuring reversibility and safety.​

Science behind Tat-MYC​​

1. Metabolic Rejuvenation – Restores the suppressed mTOR–MYC axis, reactivating glycolysis, glutaminolysis, and oxidative phosphorylation to fuel T cell growth and survival.​
2. Transcriptional Rescue – Reactivates silenced transcription factors (NFAT, AP-1, NF-κB) to drive cytokine production (e.g., IL-2, IFN-γ) and effector gene expression.
3. Checkpoint Modulation – Reverses exhaustion programs by reducing inhibitory receptors (PD-1, CTLA-4, others), enhancing persistence and cytotoxicity.
4. Functional Recovery – Together, these effects restore expansion, viral/non-viral transduction efficiency, and durable anti-tumor or anti-infective responses.
5. Stem Cell Protection & Engraftment – In hematopoietic stem cells, transient Tat-MYC exposure enhances survival through Akt–Bcl-2 upregulation and mitigates GrzB-mediated stress, supporting improved engraftment and immune reconstitution following HSCT​