CHIP refers to age-acquired somatic mutations in hematopoietic stem cells — particularly in genes TET2, DNMT3A, and JAK2 — that cause mutant blood cell clones to expand over time. These mutant macrophages and neutrophils have been shown to accumulate in atherosclerotic plaques and amplify the NLRP3 inflammasome pathway, accelerating plaque progression independently of traditional lipid-based risk factors. CHIP is now recognized as a previously unidentified, common, and potent cardiovascular risk factor — present in roughly 10% of people over 70. Importantly, studies suggest that colchicine may specifically attenuate CHIP-related cardiovascular risk by targeting the same IL-1β pathway hyperactivated in TET2-CHIP, pointing toward a future of mutation-specific cardiovascular therapy.