CFTR and Cachexia: The main findings of our investigation can be summarized as follows: 1) CFTR is normally expressed at the SR of skeletal muscle fibers and is clearly functional, as indicated by abnormal intracellular Ca2+ and contractile responses to depolarization in muscles with CFTR deficiency; and 2) diaphragm muscles lacking CFTR exhibit an exaggerated upregulation of cytokines and cachexia-inducing factors during pulmonary infection, which is associated with a major deterioration of diaphragmatic function.