The present study demonstrated that EVL was significantly upregulated in human fibrotic kidney tissues, UUO and I/R‐induced renal fibrosis mouse models as well as TGF‐β1‐ and H/R‐stimulated HK‐2 cells, while knockdown of EVL markedly reduced the mRNA and protein expression of fibrotic indicators, indicating that EVL may promote the fibrotic response of HK‐2 cells and renal fibrosis progression. The gene discussed is EVL; the disease is renal fibrosis.