Given Rac1 is overexpressed in primary ALL and AML primary blasts compared to controls [189], and pharmacological inhibition of Rac1 is selectively cytotoxic to primary ALL cells and not on normal lymphocytic cells [190], it is indeed possible that the high-level activity of STAT5 in ALL may promote Rac1- induced NOX activity helping to form a feed-forward loop analogous to AML. The gene discussed is STAT5A; the disease is acute myeloid leukemia.