To investigate the contribution of urinary K+ to symptom generation in the face of urothelial barrier dysfunction, we used a novel rat model of cystitis induced by adenoviral-mediated overexpression in the urothelium of claudin-2 (Cldn2)21, a tight-junction associated protein that forms paracellular pores and is significantly upregulated in bladder biopsies from interstitial cystitis/bladder pain syndrome (IC/BPS) patients20. The gene discussed is CLDN2; the disease is interstitial cystitis.