IFI6 and esophageal squamous cell carcinoma: To further characterize the molecular mechanism underlying overexpression of NOX4 elicited by ER stress following energy shortage, we treated IFI6-silenced ESCC cells with or without exogenous ATP and found that ATP fully rescued the increases in ATF3 and NOX4 expression induced by IFI6 silencing (Fig. 8f).