Past studies have also shown that inhibition of SF3B1 previously evaluated in the clinic against MDS, acute myeloid leukemia (AML), and chronic monomyelocytic leukemia (CMML) (29–31) blocks the growth of leukemia cells and exhibits relatively low toxicity toward normal CD34+ hematopoietic progenitors (26). This evidence concerns the gene SF3B1 and myelodysplastic syndrome.