While atRA inhibited LSC activity in FLT3-ITD bearing non-APL AML, the opposite was reported for AML expressing the AML1-ETO fusion or overexpressing EVI1. atRA strongly increased the serial replating ability of AML1-ETO expressing murine BM cells, and resulted in larger, more immature colonies [9]. The gene discussed is RUNX1; the disease is acute myeloid leukemia.