Evidence from mouse models supports the role of A20 as an endogenous inhibitor of fibrosis: fibroblast-specific deletion of A20 exacerbates bleomycin-induced skin and lung fibrosis, whereas DREAM-deficient mice, which display elevated A20 expression, are protected from fibrotic progression, highlighting the importance of the A20–DREAM regulatory axis (9). The gene discussed is KCNIP3; the disease is pulmonary fibrosis.