In patients with TET2 CHIP, proteomic profiling of atherosclerotic plaques revealed significant up-regulation of inflammatory pathways and metabolic processes, including elevated levels of CASP1, a key activator of the NLRP3 inflammasome, and concurrent down-regulation of markers associated with plaque stability.68–72 Transcriptomic analyses of monocyte-derived macrophages of CAD patients with TET2 mutations (STARNET)44,53,73 revealed profound alterations in immune and inflammatory pathways, correlating with a more complex CAD phenotype. Here, CASP1 is linked to coronary artery disorder.