Furthermore, overexpression of Gab2 in Dnmt3aR878H/+× Npm1cA/+ bone marrow led to the development of AML in 12 of 12 engrafted mice, with a median latency of 3.7 months (range, 2.3–6.3); 10 mice engrafted with an IRES-eGFP–only vector developed AML with a longer median latency of 6.2 months (range, 4.8–9.9, P = 0.0048; Figure 2G). The gene discussed is GAB2; the disease is acute myeloid leukemia.