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. The gene discussed is TET2; the disease is myelodysplastic syndrome.