Selective advantage was related to alterations in replication, segregation and survival, secondary to APC mutations acquired by the cells, initiates and drives tumorigenesis; further concomitant somatic mutations in other genes (i.e., KRAS, TP53) will follow as a consequence in a stepwise manner, accelerating the tumorigenic process along the adenoma to carcinoma sequence [23], just as for other non-hereditary tumors. This evidence concerns the gene APC and adenoma.