The past years enormous progress has been made in the understanding of the pathogenesis of myelodysplastic syndromes (MDS).1 The introduction of next-generation sequencing (NGS) and whole-exome sequencing (WES) has revealed that about 90% of patients with MDS harbor mutations in pathways such as spliceosome machinery, in epigenetic regulators and other genes previously unknown to be involved in MDS. At this year’s conference, the focus was on these mutations. There have been no major breakthroughs on the therapeutic side.

(BELG J HEMATOL 2017;8(4):146–8)