Transcriptional analysis revealed that, compared to healthy controls, cytotoxic T lymphocytes from TP53-mutated AML patients exhibited upregulation of inhibitory molecules (such as CD244, CD160, LILRB1, CD300A, and PVRIG) and downregulation of stimulatory molecules (such as CD40LG, CD28, TNFSF8, TMIGD2, and TNFRSF25). This evidence concerns the gene TP53 and acute myeloid leukemia.