Although there are a number of studies indicating that higher expression and co-expression of immune checkpoint genes such as PD-1, PD-L1, CTLA-4, and TIM-3, which induce T cell exhaustion, are associated with poor clinical outcomes for AML patients 42, 43 , it remains unclear whether alterations in T cell function genes alone or in cooperation with immune checkpoint factors contribute to T cell exhaustion and influence the clinical outcome of AML patients. This evidence concerns the gene PDCD1 and acute myeloid leukemia.