We next sought to determine if evidence of an anti-AML immune response was present in a genetically engineered knockin model of mutant Nras-driven AML, derived from mice heterozygous for conditional alleles conferring a C-terminal truncation in Npm1 and constitutively active Nras (Tg(MxI-cre), Npm1fl-cA/+; Nrasfl-G12D/+), expressed from their respective endogenous promoters31. The gene discussed is MXI1; the disease is acute myeloid leukemia.