It appears likely that immunotherapy will require use in combination with other treatments, such as hypomethylating agents i.e., SGI-110, a derivative of decitabine [47], which has been shown to lead to the re-expression of MAGE-A and NY-ESO-1 in AML blasts, or more recently treatment in a Phase II clinical trial of AML patients with azacitidine and vorinostat, which led to an increased expression of MAGE, renal cell carcinoma antigen (RAGE), LAGE, SSX2, and taxol resistance associated gene-3 (TRAG3) in blasts, which can be recognised when presented to circulating T cells [48]. This evidence concerns the gene MOK and acute myeloid leukemia.