Our findings propose that prevention of telomere attrition is such a shared mechanism, a premise that could explain: (1) the rapid rise in the prevalence of splicing-mutant CH and MDS in old age and as telomeres become critically short in at-risk people (that is, those with the shortest telomeres) and (2) the higher prevalence of splicing factor gene mutations in HSC-derived myeloid malignancies compared to any other cancer, with blood being the tissue that incurs the most marked age-related telomere shortening47. Here, SLU7 is linked to myelodysplastic syndrome.