Here, we found that an increase in PKCι expression upregulated p38 MAPK phosphorylation, which activated both p53 and c-Jun phosphorylation, resulting in the elevated expression of the TGF-β1 signaling pathway, causing renal fibrosis in db/db mice; these signals were significantly decreased by EchA treatment. The gene discussed is TP53; the disease is renal fibrosis.