Cystic fibrosis is a severe hereditary disease of the lung, for which there is currently no cure. The underlying cause of the disease is a malfunction of the chloride channel CFTR, which prevents the secretion of chloride in certain body cells. This leads to dehydration of the mucus layer in the lung. A promising approach for treating cystic fibrosis is the activation of the calcium-activated chloride channel TMEM16A as an alternative route for chloride efflux. Since TMEM16A is expressed in the same epithelium as CFTR, its activation could restore hydration of the mucus layer. TMEM16A is part of a protein family whose members facilitate the flow of negatively charged chloride ions or lipids across the cell membrane.