The most prevalent mutational subset in acute myeloid leukemia is type 1 mutations, which are present in about two-thirds of patients and result in abnormal activation and proliferation of cellular signaling pathways (e.g., FMS-like tyrosine kinase 3 (FLT3); Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS); NRAS Proto-Oncogene, GTPase (NRAS); Tyrosine-protein phosphatase non-receptor type 11 (PTPN11); neurofibromin 1 (NF1); and KIT proto-oncogene, receptor tyrosine kinase (KIT)). Here, NRAS is linked to acute myeloid leukemia.