Our novel approach designed with the intention of downregulating the Th1 inflammatory response, followed by IL-17A blockade and was based on several experimental studies evaluating anti-IL-17 therapy, in which worsening of colitis in patients21 or glomerulonephritis in animal models34 was observed in the presence of an active Th1 pro-inflammatory response. The gene discussed is IL17A; the disease is glomerulonephritis.