Clonal hematopoiesis (CH) involves a single hematopoietic stem/progenitor cell (HSPC) gaining a selective advantage due to somatic mutations, increasing the risk of hematological malignancies and cardiovascular disease. In murine models of CHIP with Tet2 deletion, the proinflammatory cytokine IL1β promotes the expansion of pro-inflammatory monocytes/macrophages and hinder demethylation of enhancers and transcription factor binding sites associated with lymphoid and erythroid differentiation. This work suggests that IL1β enhances the self-renewing ability of Tet2-deficient HSPCs by upregulating self-renewal genes and resisting demethylation, highlighting IL1 signaling as a potential target for early intervention in preleukemic disorders.