In support of this, our group recently published that ER stress in colon-derived enteroid monolayers drives inappropriate TLR5 responses leading to the expression of unidentified factors that mature dendritic cells (DCs) to become pro-inflammatory—describing a novel pathway that may lead to the inappropriate anti-commensal inflammatory responses seen in IBD (Rees et al., 2020b). Here, TLR5 is linked to inflammatory bowel disease.