However, aCML cases have been reported to be associated with mutations of spliceosome proteins, e.g. in U2AF1, of epigenetic modifiers, e.g. in ASXL1, TET2, EZH2, and of signaling molecules, e.g. in NRAS, KRAS, JAK2, CSF3R [19]. The gene discussed is NRAS; the disease is atypical chronic myeloid leukemia, BCR-ABL1 negative.