The therapeutic potential of autophagy augmenting drugs has been extensively investigated in controlling chronic CF lung disease and associated pulmonary infection-related exacerbations. There have been extensive studies on the use of rapamycin in controlling CF-related lung infections, but its clinical use is hampered due to its potent immunosuppressive property and certain reports of significant lung toxicity [5,6,44,151,153,202]. Lately, the efficacy of the thymic peptide, Thymosin α-1 (Tα1), was demonstrated in correcting the basic defect in CF, which is the restoration of misfolded ΔF508-CFTR to the PM [203]. Tα1 possesses anti-inflammatory properties and is also known to induce autophagy [204], which could be its mechanism of action to rescue ΔF508-CFTR. Nonetheless, future pre-clinical and clinical studies will be essential before it could be any therapeutic benefit in CF-related autophagy dysfunction and exacerbations. The utility of cysteamine, a potent antioxidant drug with autophagy-inducing potential, has been widely tested in CF in vitro, in vivo models, and is currently being investigated in phase 2 human clinical trials [58,205,206,207]. However, a previously completed study of 10 patients with the ΔF508-CFTR mutation demonstrated a significant improvement in CFTR function with cysteamine treatment [208]. Similarly, our recent studies validated cysteamine’s extensive repertoire of protective mechanisms in CF, and demonstrated for the first time that cysteamine was able to control CS-induced lipophagy impairment and the resulting ceramide accumulation in murine lungs [22]. This finding might have implications in controlling both COPD and CF-related infections and exacerbations, knowing the deleterious role of ceramide in promoting pulmonary infections in COPD and CF.