In the UUO model, we found that whereas CB1 expression was drastically increased in the tubules, interstitium and glomeruli, CB1R blockade significantly reduced the increase of renal fibrosis through a direct paracrine/autocrine role of CB1R in myofibroblasts with no strong evidence for a direct role of CB1R expressed in tubules (12). The gene discussed is CNR1; the disease is renal fibrosis.