From this summary, the most frequently mutated genes in aCML patients appear to be ASXL1, NRAS, SETBP1, SRSF2 and TET2. In addition to broad cytoreductive and supportive measures (Schwartz and Mascarenhas, 2019[14]), clinical responses with inhibitors of mutated NRAS and FLT3 have been observed in single cases validating this individualized approach (Khanna et al., 2015[7]; Langabeer et al., 2017[8]). Here, NRAS is linked to atypical chronic myeloid leukemia, BCR-ABL1 negative.