In vivo treatment with OCA has been shown to effectively ameliorate BLM-induced pulmonary function loss and reverse lung fibrosis by attenuating EMT, reducing IL-6 and IL-1β, and downregulating profibrotic SNAI1 and TGF-β1 expression [92], even superior to those obtained with pirfenidone [93], highlighting FXR as a novel PF therapeutic target. The gene discussed is TGFB1; the disease is pulmonary fibrosis.