T cells can modulate their cellular metabolism according to their functional needs.34 However, this metabolic switch can be altered by the TME which can lead to T cell dysfunction.42 Along with the induction of a less differentiated phenotype and enhanced effector functions, our results showed that Δ133p53α is associated with a metabolic reprogramming in tumor-reactive engineered CD8+ T cells characterized by a quiescent metabolic state with lower glycolytic activity and expression of GLUT1. This evidence concerns the gene SLC2A1 and neoplasm.