The immune-infiltrated microenvironment that was characterized by severe immune suppression (high expression of PD-L1, CTLA4, IDO1 and BTLA), higher dependence from IFN-γ driven adaptive immune responses, high T-cell infiltration and expression of major histocompatibility complex, closely clustered with the adverse-risk genetic AML categories (specifically, TP53 and RUNX1 mutated AML) [129]. Here, IFNG is linked to acute myeloid leukemia.