A GWAS meta‑analysis of more than 640,000 individuals identified a rare noncoding variant, rs17834140‑T, that lowers risk of clonal hematopoiesis of indeterminate potential (CHIP) and subsequent blood cancers by weakening MSI2 RNA‑binding activity. Gene‑edited human hematopoietic stem cells showed the variant disrupts a GATA‑2 binding site and reduces stem‑cell clonal expansion, offering a molecular explanation for inherited resilience to clonal growth. Published in Science, the work links an inherited regulatory change to reduced somatic clonal expansion and suggests MSI2 as a potential pan‑cancer therapeutic target. The study provides human genetic evidence that modulation of RNA‑regulatory programs in stem cells can alter age‑related cancer risk and supports ongoing preclinical MSI2 inhibitor programs.