Mutations in RUNX1 are commonly associated with AML but are also found in B-ALL and T-ALL, and are usually inactivating, suggesting that RUNX1 normally functions as a tumor suppressor (Blyth et al., 2005; Mangan and Speck, 2011; Zhang et al., 2012). The gene discussed is RUNX1; the disease is acute myeloid leukemia.