Yet, the defective intracellular trafficking of ADAM22 variants (e.g. Pro438Thr and Gly448Asp) is similar to that of ΔPhe508-CFTR in cystic fibrosis and LGI1 mutants in ADLTE.21,37 Chemical correctors including chemical chaperones and proteostasis regulators effectively correct defective CFTR and LGI1 folding and increase their cell-surface expression and secretion, respectively.21,38,39 Therefore, it might be possible that some ADAM22 mutant proteins can be chemically corrected. This evidence concerns the gene ADAM22 and cystic fibrosis.