We have shown using a murine model of AML, specifically MLL-ENL, that Hhex was required for both the initiation and propagation of AML, with loss of Hhex resulting in the upregulation of p16INK4a and p19Arf, leading to myeloid differentiation and growth arrest (86). The gene discussed is KMT2A; the disease is acute myeloid leukemia.