ER stress and UPR had been shown to be closely associated with inflammatory bowel disease and CRC [65], Yugang Wang etc. revealed that high expression of PERK contributed to increased tumor vascular density and tumor growth by activating the UPR, which promoted the production of pro-angiogenic mediators and reduced the production of pro-angiogenic inhibitors [66]. This evidence concerns the gene EIF2AK3 and colorectal carcinoma.