RUNX1 and myelodysplastic syndrome: This finding is in agreement with the concept that the development of AML requires concerted cooperation of different molecular genetic alterations.[11, 20] Intriguingly, patients with SF mutations had significantly higher incidences of RUNX1, ASXL1, IDH2 and TET2 mutations than those without the mutation, similar to the findings in MDS.[4, 6, 18, 19]