Intracellular endoplasmic reticulum stress response and autophagic dysfunctionality, dysregulation of Th1 and Th2 mediated responses, chronic inflammatory responses induced by IL-23, expansion of Th17 cells (derived from TGF-beta and IL-6) and epithelial TNF-induced apoptosis are several pathways involved in IBD (Geremia et al., 2014; Larabi et al., 2020). This evidence concerns the gene IL37 and inflammatory bowel disease.