Accordingly, phenotypically high expression of growth factor receptors, such as IL-3 receptor (CD123), c-kit, and FMS-related tyrosine kinase 3 (FLT3), or genetic mutations in these receptors or their downstream pathways, such as neuroblastoma RAS viral (v-ras) oncogene homolog (N-RAS), were observed in the LSCs of AML, which incurred the overactivation of their downstream tyrosine kinases [11,12,13]. The gene discussed is NRAS; the disease is acute myeloid leukemia.