Moving beyond the risk of overt hematologic malignancy, the altered inflammatory milieu imposed by CH promotes systemic inflammation and increased morbidity and mortality.1,17-20 Several studies of CH have characterized a hyperinflammatory environment, including elevated levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β through the activation of various inflammatory pathways.1,17-20 The effects of DNMT3A and TET2 mutations have been best characterized in relation to inflammation, although knowledge is still incomplete. The gene discussed is IL1B; the disease is cyclic hematopoiesis.