Recent studies suggest, however, that perturbations of BCOR function alone do not suffice to induce malignant transformation [10,21,44], and thus co-mutations appear to be needed in order to drive leukemogenesis or, alternatively, sequential, secondary acquisition of LOF in BCOR following an oncogenic event, e.g., MDS driver mutation triggers disease progression towards AML, as suggested by the higher frequency of sAML among mBCOR patients. The gene discussed is BCOR; the disease is acute myeloid leukemia.