Genetic depletion of SQSTM1, transgene-enforced BECN1 overexpression, or addition of autophagy-stimulatory proteostasis regulators, such as cystamine (or its reduced form cysteamine), can increase the expression level of F508del-CFTR protein and restore its function at the PM, either in CFTR homozygous CFBE41o- bronchial epithelial cell lines or in primary nasal epithelial cells freshly collected from CF patients bearing F508del-CFTR mutation, as well as in the lungs from CftrF508del mice [34, 35]. This evidence concerns the gene CFTR and cystic fibrosis.