Although the precise mechanism by which morphine may induce epithelial disruption remains unknown, a role of μ-opioid receptors (MOR) and toll-like receptor (TLR) signaling has been proposed [36,37]: in murine models for colitis, MOR activation led to the activation of inflammatory responses through an increased migration of immune cells and TLR-mediated disruption of tight junctions [37]. This evidence concerns the gene OPRM1 and colitis.