Tet2-deficient hematopoietic cells have increased levels of proinflammatory cytokines such as IL-1β and IL-6, and humans with TET2-mutant CHIP have elevated levels of IL-1β.3,4,15,39 In mice, Nlrp3 inhibition, which results in decreased activation of IL-1β, attenuates hematopoietic Tet2KO-driven atherosclerosis, HF, liver fibrosis, and gout.4,27,34,35 As noted, lethally irradiated Ldlr−/− mice with hematopoietic-specific inactivation of Tet2 showed markedly higher atrial Nlrp3 expression compared with WT controls (Figure 2G). This evidence concerns the gene IL1B and gout.