Consequently, with the incidence of retinopathy and nephropathy inextricably linked [20], here we utilise an in vivo model of advanced interstitial inflammation and fibrosis and determine that genetic deletion of tubule-specific Cx43 (Pax8-rtTA- cre:cx43 flox Cx43−/−) or pharmacological inhibition of Cx43-hemichannel activity using the Cx43 specific hemichannel inhibitor Peptide5 [21], preserves tubule structure, reduces interstitial fibrosis and attenuates NLRP3 inflammasome activity and inflammation in the face of UUO. The gene discussed is GJA1; the disease is inflammatory response.