In addition to the abnormal myeloid differentiation (gene rearrangements in RUNX1, CBFB, RARA, and alterations in other transcription factors), it has become evident that more than 95% of AML patients carry known driver and co-occurring mutations that are implicated in the survival of the neoplastic clone or subclones (Gupta, 2016; Papaemmanuil et al., 2016). The gene discussed is RUNX1; the disease is acute myeloid leukemia.