Three main pathways have been described for the formation of sporadic CRC tumors: (I) the adenoma–carcinoma sequence, influenced by chromosomal instability (CIN), microsatellite instability (MSI), KRAS, APC, and Tp53 mutations; (II) the serrated pathway, governed by the methylation of CpG island methylator phenotype (CIMP), MSI, BRAF, and CDKN2A mutations; and (III) the inflammatory pathway, related to the activation of inflammatory signaling pathways such as NFκB, IL-6/STAT3, COX-2/PGE2 and IL-23/Th17 [5,6]. This evidence concerns the gene TP53 and colorectal carcinoma.