Considering the mucus lowering effects of CPZ and importance of TRPA1 and TRPV1 in the gut mucin-immune axis, we hypothesize that using CPZ (for inhibiting or desensitizing TRPV1 and TRPA1 nociceptors) as a strategy for the treatment of IBD-associated pain might impair colonic mucin homeostasis, leading to increased gut permeability and dysbiosis. The gene discussed is MUC5AC; the disease is inflammatory bowel disease.