The spontaneous relapse seen after mimicking RAS oncogene-targeted cancer therapy closely resembles the major clinical challenge for targeted cancer therapies in general,15, 16, 17, 18, 19, 20, 21, 22, 39, 40 and confirm that NRAS(V12)-addicted AML cells can acquire alternative mechanisms for maintained growth and survival and survive in the absence of the NRAS oncogene. This evidence concerns the gene NRAS and acute myeloid leukemia.