Additionally, acute myeloid leukaemia (AML) cells are known to overexpress PD-L1 [119] and IDO1 [120], and AML blasts can secrete arginase II in order to promote immune escape by suppressing T-cell proliferation and polarizing monocyte differentiation towards an M2 phenotype [121]. This evidence concerns the gene CD274 and acute myeloid leukemia.