TGF‐β‐mediated tissue fibrosis relies on a persistent feed‐forward mechanism of EGFR/ERK activation.[25] To explore the effects of Glce in the pathogenesis and progression of renal fibrosis in vivo through the EGFR/ERK signaling pathway, the EGFR inhibitor, erlotinib, was administered post‐UUO (Figure5A). This evidence concerns the gene EGFR and renal fibrosis.