Similarly, transport of acid-base equivalents coupled to Cl− has been convincingly shown to modify blood pressure: knockout of the anion-exchanger pendrin (Slc26a4), which contributes to Cl− reabsorption in the distal nephron (Wall et al., 2004), has been shown to protect against mineralocorticoid-induced hypertension (Verlander et al., 2003) while overexpression of pendrin in the intercalated cells was recently shown to cause hypertension (Jacques et al., 2013). The gene discussed is SLC26A4; the disease is hypertensive disorder.