CFTR and Alzheimer disease: Misfolding diseases feature overexpression of aggregation—prone proteins such as Aβ in AD, α-synuclein in PD, or huntingtin in HD that entail a “toxic-gain-of-function” resulting in chaperome overload, gradually exceeding proteostasis capacity [77], while “loss-of-function” misfolding diseases feature specific perturbations such as dysfunctional ∆F508-CFTR in cystic fibrosis [78].