The authors described that MDS “founder” lesions recurrently affected genes involved in the regulation of DNA methylation (e.g., TET2, DNMT3A), chromatin remodeling (e.g., ASXL1), or RNA splicing (e.g., SF3B1), and that del(5q) was acquired as a secondary lesion or constituted a minor independent clone in 62% of patients classified as MDS-5q. Here, ASXL1 is linked to myelodysplastic syndrome.