However, the contribution of HDAC to AML pathogenesis has been linked to aberrant recruitment of these enzymes by myeloid oncoproteins such as AML1-ETO, PML-RARA, and EVI1 (Izutsu et al., 2001; Senyuk et al., 2002; Hug and Lazar, 2004; Falkenberg and Johnstone, 2014). Here, RUNX1 is linked to acute myeloid leukemia.