ATF4 and nasopharyngeal carcinoma: Gambogenic acid opened chloride channels and activated VSOR Cl− channels, leading to the efflux of VSOR Cl− currents, a decrease in the levels of ERS-related protein GRP78 and an increase in CHOP and ATF4 expression levels; the primary mechanism behind these processes was the overexpression of CHOP, which repressed the anti-apoptotic impact of the UPR and triggered apoptosis in the CNE-2Z cell line of nasopharyngeal carcinoma (Su et al., 2019).