Jaiswal et al. report the results of four case–control studies that confirm a near doubling in the risk of coronary heart disease in patients with CHIP,1 a finding that was first reported in the Journal in 2014.2 The authors postulate that two mechanisms may be involved: the promotion of inflammatory responses, as supported in a study involving Tet2 knockout mice, and an increase in the number of myeloid cells, a finding that appears to be more relevant for patients with JAK2 mutations, which confer a much larger risk than the more common DNMT3A, TET2, and ASXL1 mutations, in which blood counts remain normal. However, the authors do not provide data relating to red-cell distribution width, which is the only blood-cell index that has been shown to have a significant association with CHIP2 and which has been associated with an unexplained increase in all-cause mortality in an aging population. 3,4 In understanding how CHIP promotes atherosclerosis, it is important to explore the causal relationship between clonal hematopoiesis and red-cell anisocytosis to determine whether these are independent or associated risk factors for cardiovascular disease.