EGFR was a key target for molecular therapy, involved in the regulation of cell metabolism, growth, migration, and differentiation, which was overexpressed in various tumors such as prostate cancer, breast cancer, and colon cancer.36 Meanwhile, a previous study showed that loss of p53 could cause the increased activity of EGFR promoter, and further increase the expression of EGFR.37 In consistence with the result, our study showed that EGFR was up‐regulated accompanied by down‐regulation of p53 in CHI3L1 overexpressed cells. The gene discussed is EGFR; the disease is prostate carcinoma.