Indeed, co-expression of an AML-associated, constitutively active NrasG12D mutant significantly promoted kinetics of ZM-induced AMLs (Fig. 1h, with an average latency of 41 days for the “ZM + Nras” cohort)—during disease progression, leukemia cells co-expressing ZM and NrasG12D (luciferase-labeled) homed to and expanded in bones and spleen (Fig. 1r and Supplementary Fig. 2a). Here, NRAS is linked to acute myeloid leukemia.