Secondary hits that contribute to clonal expansion and cytopenia development are frequently seen in SETBP1, RUNX1 and EZH2, while subclonal events that promote leukocytosis and drive eventual AML progression frequently affect RAS pathway genes (N/KRAS, CBL, PTPN11 and FLT3) [3,4,35] (Figure 3B). The gene discussed is RUNX1; the disease is acute myeloid leukemia.