Notably, CF cell lines and CFTR knockout animal studies indicate that the loss of CFTR is sufficient to generate a proinflammatory environment [62], which can lead to the ROS-mediated activation of transglutaminase-2 (TGM-2) and the inactivation of the Beclin-1 complex, resulting in autophagy impairment [55,63,64]. Here, BECN1 is linked to cystic fibrosis.