Therefore, to determine the necessity of the enzymatic function of Glce in EGFR activation and TGF‐β1‐induced EMT during renal fibrosis pathogenesis, we selected three critical sites for the enzyme activity including, Y500, Y560, and Y578, for mutational studies.[12] HK‐2 cells with stable Glce knockdown were transfected with plasmids containing mutant genes. Here, EGFR is linked to renal fibrosis.