HLA-C and acute myeloid leukemia: Only a few new drugs have been developed for AML that have significantly altered patient outcomes—of these epigenetic modifiers such as azacitidine and vorinostat appear amongst the most promising.1, 2 One proposed mechanism of action is the upregulation of MHC‐restricted previously undetectable cancer‐testis antigens (CTAG) allowing antigen‐specific T cells to recognise and kill AML blasts.3 However, attempts to trigger autologous T cell responses have led to only limited clinical improvements, with the mechanism of failure poorly understood.