In contrast, a variety of mutations in epigenetic modifiers (TET2, DNMT3A, IDH1/2), transcription factors (TP53, RUNX1, IKZF1), and splicing factors (SF3B1, U2AF1, SRSF2) have been identified and assigned a role in progression from ET or PV to sMF or from MPN-CP to MPN-BP, with an associated myelodysplastic phenotype that increases with the number of these mutations [4]. The gene discussed is TP53; the disease is myeloproliferative disorder.