Gain- and loss-of-function experiments exhibited that overexpression of KCNQ1OT1/XIST weakened ERS activation-induced cell apoptosis, and partly abolished XBP-1u knockdown-caused cell viability loss and cell apoptosis, suggesting that targeting XBP-1-mediated ERS response using KCNQ1OT1 or XIST might be a promising strategy for CRC treatment. This evidence concerns the gene XIST and colorectal carcinoma.