In addition, PAR‐1 may also directly potentiate the intrinsic migratory activity of macrophages.26, 29 Once recruited, macrophages secrete large amounts of pro‐fibrotic cytokines like TGF‐β, which in turn induce fibroblast proliferation.7, 30 It is thus tempting to speculate that reduced macrophage recruitment in PAR‐1‐deficient mice results in the observed reduction in fibroblast accumulation with subsequent reduced extracellular matrix production and renal fibrosis. The gene discussed is TGFB1; the disease is renal fibrosis.