Consistent with these results, overexpression of FGFR4, the specific receptor for fibroblast growth factor (FGF)‐1 and FGF‐3, was associated with epithelial‐to‐mesenchymal transition, tumor progression, and drug resistance of CRC.27, 28 The results from this study demonstrated that ablation of FGFR4 effectively blocked AOM/PM‐induced experimental CRC in mice, suggesting that the PI3K/AKT cascade plays an important role in PM‐involved colonic tumorigenesis. The gene discussed is AKT1; the disease is colorectal carcinoma.