AML blasts evade immune surveillance by disrupting the immune microenvironment through multiple mechanisms, including downregulation of human leukocyte antigen class I and II presentation and upregulation of the immune checkpoint inhibitors programmed death ligand-1 (PD-L1), T-cells immunoglobulin-mucin 3 (TIM-3), and C-lectin-like inhibitory receptor-4 (CTLA-4) [49]. Here, CTLA4 is linked to acute myeloid leukemia.