As a proof of concept, numerous recent studies have demonstrated the potential of targeting CFTR-autophagy dysfunction as a method for reducing recurrent exacerbations. One drug that has shown promise in alleviating autophagy impairment to provide possible therapeutic benefits in the treatment of exacerbations is cysteamine. Cysteamine is an FDA approved drug for the treatment of cystinosis; however, it also possesses antioxidant, anti-inflammatory, autophagy-inducing, mucolytic, and anti-bacterial properties [58,205,207]. Recently, Ferrari et al. demonstrated that cysteamine could re-establish P. aeruginosa clearance in macrophages with the ΔF508-CFTR deletion by salvaging ΔF508-CFTR function in macrophages [58]. This restoration of function allowed macrophages to both increase the internalization and clearance of P. aeruginosa via a Beclin-1-mediated initiation of the autophagy pathway [58]. This reveals a possible therapy to restore both CFTR and autophagy function in CF patients that could limit P. aeruginosa colonization. An improved clearance of P. aeruginosa in CF patients is especially important due to the prevalence of P. aeruginosa infections in exacerbations, and a drug that improves the immune response in this way offers a method to decrease exacerbations.