Next generation sequencing (NGS) studies have shed some light on the clonality of the disease, (i) showing that MDS founding clones contain mutations which persist when patients progress to AML3,4, and (ii) that commonly mutated genes such as DNMT3A, TET2, ASXL1, TP53 and SF3B1, are important for initiating the disease5,6. This evidence concerns the gene SF3B1 and myelodysplastic syndrome.