Disruption of ER-to-Golgi trafficking or ER stress promotes F508del CFTR transport to the plasma membrane through Golgi-bypassing secretory autophagy in a GRASP55-dependent manner.426,432 Notably, the F508del CFTR delivered through the unconventional secretion pathway exhibits sufficient functionality,429 suggesting that restraining ERAD and promoting trafficking of mutant forms of CFTR to the cell surface represent another therapeutic intervention targeting cystic fibrosis. This evidence concerns the gene CFTR and cystic fibrosis.