Having demonstrated efficient cooperation of the E177R partial-LOF mutation with oncogenic Ras in two solid tumor models, we next explored this cooperation in a model of acute myeloid leukemia (AML), which is driven by the combination of NrasG12D and AML1/ETO9a oncogenes and in which p53 is known to be tumor suppressive [37]. The gene discussed is TP53; the disease is neoplasm.