The increased expression of immune checkpoints, such as programmed death 1 (PD-1), cytotoxic T-lymphocyte antigen 4 (CTLA4), T-cell immunoglobulin and mucin-domain containing-3 (TIM-3), and lymphocyte-activation gene 3 (LAG3), contribute to AML immune evasion and are associated with disease progression and relapse (reviewed by [118]). This evidence concerns the gene HAVCR2 and acute myeloid leukemia.