Not surprisingly, targeting properdin, either genetically or pharmacologically, has been shown to effective in countering a number of renal diseases where properdin is elevated, including hemolytic uremic syndrome, ANCA-associated vasculitis, C3 glomerulopathy, IgA nephropathy, renal transplantation and murine model of acute anti-glomerular basement membrane disease (36–45). This evidence concerns the gene CFP and hemolytic-uremic syndrome.