NRAS and acute myeloid leukemia: Npm1c/NrasG12D AML cells generated a rapid, fully penetrant AML when transplanted into Rag2−/−γc−/− recipients, however there was a marked delay in disease latency in immunocompetent WT recipients (Fig. 2F, G), confirming an intrinsic immune response to a genetically engineered AML mouse model driven by mutant Nras.