Remarkably, a unique dependence on SOS1 in KRASG12D-induced leukemogenesis has also been previously reported based on the detection of SOS1 overexpression in KRASG12D/+ cells and the observation that SOS1 deletion ameliorates oncogenic, KRAS-induced myeloproliferative neoplasm (MPN) phenotypes and prolongs the survival of KRASG12D/+ mice [47]. The gene discussed is KRAS; the disease is myeloproliferative neoplasm.