The transformation of chronic-phase MPN to secondary acute myeloid leukemia (sAML) is a severe complication traditionally linked to the acquisition of additional mutations in the MPN driver clone in genes encoding epigenetic regulators (e.g. TET2, DNMT3A, ASXL1), tumor suppressors (e.g. TP53, JARID2) and signaling molecules (e.g. N/K-RAS)7–10. Here, KRAS is linked to myeloproliferative neoplasm.