Our previous study [11] also showed that, in CRC cell lines, the overexpression of TRIP13 drives metastasis through epidermal growth factor receptor (EGFR) activation, interaction with fibroblast growth factor receptor 4 (FGFR4), activation of the Wnt signalling pathway and the epithelial–mesenchymal transition (EMT), regardless of cell p53, KRAS, BRAF and microsatellite instability (MSI) status, suggesting that it is a potential target for the treatment of CRC. This evidence concerns the gene KRAS and colorectal carcinoma.