Today, thanks to molecular, genomic, and genetic studies, we know that dysregulation of many genes contributes to the development of CRC, such as the APC gene, which leads to the activation of the Wnt/β-catenin pathway and contributes to the initiation of the neoplastic process; TP53 and PIK3CA pathways, which contribute to the progression of CRC; and the SMAD4 and TGF-β pathways, whose involvement in metastasis has also been described [4]. This evidence concerns the gene TGFB1 and colorectal carcinoma.