Although somatic mutations are less frequent in blood malignancies compared to solid tumors (87), they often can be linked to altered gene function implicated in tumorigenesis such as mutations in TET2 (88), DNMT3A (89) (MDS/AML), SF3B1 (90, 91) (CLL, MDS) or JAK2 (92) (MPN) and acquired therapeutic resistance (BCR-ABLT315i, BTKC481S, PLCG2R665W) (93, 94) (Figure 1D). This evidence concerns the gene SF3B1 and myelodysplastic syndrome.