Over the past three decades, molecular genetic studies have revealed some critical mutations underlying the pathogenesis of the sporadic and inherited forms of CRC [4], including mutational inactivation of the adenomatous polyposis coli (APC) tumor suppressor [5], resulting in overactivation of the Wnt/β-catenin signaling pathway, dysregulated cell proliferation and adenoma development [6], or microsatellite instability, assessed with the detection of mono- and di-nucleotide tracts selected by the National Cancer Institute consensus conference [4,7]. The gene discussed is APC; the disease is colorectal carcinoma.