The overexpression of Hoxb2 and Hoxb3 in mouse pro-B cells resulted in decreased FLT3-ITD-dependent cell proliferation, reduced colony formation, and increased apoptosis, suggesting that HOXB2 and HOXB3 are regulators of FLT3-ITD-driven AML [77]. The gene discussed is FLT3; the disease is acute myeloid leukemia.