ANO1 and renal fibrosis: The mechanism regarding TMEM16A mediating the elevation of [Cl]i in renal fibrosis has not yet been fully elucidated, and may be due to 1) differences in Cl− concentration on renal tubular epithelial cells that predispose to inward flow, 2) indirect regulation of other Cl− reabsorption pathways, 3) pathological conditions may shift Cl− outflow to influx when the membrane potential reaches the Cl− reverse potential (Deba and Bessac, 2015).