Although the random population-level sampling of the FINRISK study and the hospital-based recruitment in FinnGen provided complementary cohorts to evaluate the association between CH and RA, the limited cohort size of FINRISK and the absence of NGS data in FinnGen highlight the need for further analyses of the link between CHIP and prevalent autoimmune disease in other populations and cohorts. This evidence concerns the gene STUB1 and cyclic hematopoiesis.