Differential expression of TLR subtypes has been reported in IBD patients [266, 267] and strikingly, absence of TLR4, for which polymorphisms have been documented in IBD [268, 269] and which is expressed by enteric neurons and EGCs [270–272], affects S100B and GFAP expression and enhances inhibitory neurotransmission and neuronal death through the interaction of NO with purinergic signaling in murine models [273, 274]. Here, GFAP is linked to inflammatory bowel disease.