In fact, the rescue of dysfunctional autophagy in CF, mediated by autophagy inducers such as MTOR inhibitor (rapamycin), TG2 inhibitor (cistamine), and/or modulators of Ca2+-dependent signaling (KB-R7943), attenuated the hyperinflammation in CF lung, improving the CFTR transport to PM and reducing ROS production and cytokine release in macrophages and in primary CF airway cells in vitro and in CF mouse models in vivo (127–132). Here, CFTR is linked to cystic fibrosis.