A recent study demonstrated that activated PKCα accelerated renal fibrosis development by increasing the expression of LAMP-2, autophagosome-lysosome fusion and autophagy flux, which was abolished by PKCα inhibitor Go6976 and PKCα-siRNA in the TGF-β-induced fibroblasts and UUO-stimulated mouse model 150. The gene discussed is TGFB1; the disease is renal fibrosis.