Cystic fibrosis (CF) is a disease of protein homeostasis (proteostasis) that arises from the defective biosynthesis, folding, and/or function of a chloride channel known as the cystic fibrosis transmembrane conductance regulator (CFTR).1,2 The most common CF mutation (ΔF508) induces CFTR misfolding by decoupling the folding of its subdomains during translation.3,4 This cotranslational misassembly reaction enhances the retention and degradation of the CFTR protein within the endoplasmic reticulum (ER) and ultimately reduces the trafficking of the functional protein to the plasma membrane. Here, CFTR is linked to cystic fibrosis.