In three different models of CKD (i.e., the transgenic renin [Ren+/+] model, the administration of antibody against the glomerular basement membrane [α-GMB] and the unilateral obstructive uropathy), Toubas et al. observed an increase in the renal amounts of Cx43, so they postulated that the change in this Cx was caused by the development of inflammation in the damaged kidney [34]. The gene discussed is REN; the disease is urinary tract obstruction.