Caffeine has been shown to antagonize TGF-β-induced Smad signaling in a concentration-dependent manner in lung epithelial cells and reduced collagen deposition in an ex vivo precision-cut lung slice model of pulmonary fibrosis, suggesting that caffeine inhibits profibrotic effects of TGF-β (109). The gene discussed is TGFB1; the disease is pulmonary fibrosis.