The latter include mutations of receptor tyrosine kinases [KIT proto-oncogene-receptor tyrosine kinase (KIT) and fms related receptor tyrosine kinase 3 (FLT3)], intracellular kinases [e.g., Janus kinase 2 (JAK2)], ASXL transcriptional regulator 1 (ASXL1), and GTPases [e.g., the neuroblastoma RAS viral oncogene homolog (NRAS) Kirsten rat sarcoma viral oncogene homolog (KRAS)], which are all frequently associated with a poor response to standard AML chemotherapy[5,40-49]. Here, NRAS is linked to acute myeloid leukemia.