Recent gene essentiality profiling demonstrated that NRAS and KRAS mutations are driver oncogenes in AML, as attested by the dependency of RAS mutated AML cells on NRAS or KRAS expression, and by the discovery of synthetic lethal interactions between oncogenic RAS and effectors of RAS maturation or MAPK signaling that are exclusively found in RAS mutant AML cells [4]. The gene discussed is NRAS; the disease is acute myeloid leukemia.