Although great advances have been made in the understanding of ER stress, the regulatory mechanism for deregulation of ER stress in IBD remains unclear.19 In this study, we found that miR-665 was upregulated in IBD samples, and substantially repressed the components of ER stress, XBP1 and ORMDL3, leading to enhancing apoptosis by activation of JNK. The gene discussed is MAPK8; the disease is inflammatory bowel disease.