Treatment of mice bearing the Cftrdel506 mutation with a combination of EGCG (an inhibitor of the autophagy repressor EP300) and cysteamine (which restores the trafficking of CFTRdel506 to the membrane by inhibiting TGM2 [transglutaminase 2, C polypeptide]) yield to tangible clinical and preclinical benefits in autophagy‐competent mice, yet fail to do so in their autophagy‐deficient counterparts, further emphasizing the key involvement of autophagy in CF pathogenesis (Tosco et al, 2016). Here, TGM2 is linked to cystic fibrosis.