Despite the overlap in the genetic profile, the events accompanying leukemic transformation are not identical between the two disorders: post-MDS sAML is mainly initiated upon acquisition of mutations in: proteins involved in signaling (eg, K-Ras, N-Ras and FLT3), transcription factors (RUNX1, GATA2, CEBPA), or nucleophosmin 1 (NPM1) [98]. This evidence concerns the gene FLT3 and myelodysplastic syndrome.