Downregulation of TLR4 and its downstream signaling shifts macrophage polarization from an M1 towards an M2 phenotype and ameliorates renal interstitial fibrosis, glomerulosclerosis, and renal functional loss in the early stages of UUO [34] and adriamycin nephropathy in rats [35]. The gene discussed is TLR4; the disease is glomerulosclerosis.