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There are many theories have emerged to explain the pathogenicity of IC/BPS, including mast cell activation, neurogenic inflammation, urinary tract infection, tight junction protein downregulation, afferent nerve plasticity, bladder epithelial dysfunction, urothelial signaling disturbances, autoimmune disorders, high urothelium permeability, pelvic floor dysfunction, and psychosomatic factor.[2] Although the clinical characteristics of IC/BPS are largely unknown, there are accumulated evidences on possible theories for its etiology, pathophysiology, and epidemiology.[3] This complexity leads to uncertain diagnoses, which consequently leads to ineffective treatment