In this context, our current vision is that the loss of ICCs expressing muscarinic M3 receptors in TNBS-induced ileitis contributes to reduce extracellular adenosine accumulation, breaking down the amplification loop initiated by ACh release from myenteric neurons that is mediated by muscarinic M3 receptors-induced adenosine overflow from ICCs, and concluded through the activation of facilitatory A2A receptors on cholinergic nerve terminals. Here, CHRM3 is linked to Crohn ileitis.