Experimental studies further showed that <i>TET2</i> deficiency promoted macrophage lipid accumulation and inflammatory activation and induced endothelial dysfunction, supporting the biological relevance of the cerebrovascular and cardiometabolic associations.<h4>Conclusions</h4>CHIP is associated with subtype-specific patterns of cerebrovascular risk within a broader cardiometabolic context. This evidence concerns the gene TET2 and endothelial dysfunction.