STAT5 binds and activates Rac1, promoting NOX mediated ROS production, to increase DNA damage in AML cell lines [30], a possible mechanism by which ETV6/RUNX1 induces ROS and garnishes the secondary hit necessary for preleukemic clones to propagate mutations that favour the development of fully transformed ALL. The gene discussed is STAT5A; the disease is acute myeloid leukemia.