This continuous activation leads to metabolic shifts, reduced cytokine production, impaired cytotoxicity, and increased inhibitory receptors like PD‐1, CTLA‐4, and TIM‐3.[23] Epigenetic changes, such as histone modifications, further contribute to CAR‐T dysfunction by dysregulating genes essential for activation, survival, and memory.[24] Unlike regular T cells, which are activated by external stimuli, CAR‐T cells experience sustained activation within the immunosuppressive tumor microenvironment, intensifying epigenetic alterations and exhaustion.[25]. This evidence concerns the gene HAVCR2 and neoplasm.