New research has examined the role of Ca2+-dependent Cl transport in the kidney, focusing on the channel anoctamin 1 (Ano1). Immunohistochemistry revealed that Ano1 is predominantly expressed in the proximal tubular epithelium. Indeed, tubular Ano1 knockout led to proteinuria whereas selective knockout in podocytes did not have an effect on renal function, suggesting that Ano1 has a role in protein reabsorption rather than in the glomerulus. Low pH activated Ano1 currents, implicating Ano1-mediated Cl secretion in effective H+ transport by the vacuolar-ATPase in the kidney.