Acute myeloid leukemia (AML) is a complex disease driven by multiple cytogenetic abnormalities, such as inv(16), t(8;21), t(15;17), 3q abnormalities, deletions of (the q-arms) of chromosome 5 and 7 and by aberrant expression and/or mutations of genes e.g., EVI1, FLT3, RAS, RUNX1, CKIT, WT1, CEBPA and NPM1[1], [2]. Here, RUNX1 is linked to acute myeloid leukemia.