APC and colorectal cancer: The loss of function by inactivating mutations in the adenomatous polyposis coli (APC) or axis inhibition protein (axin) tumor suppressor proteins or activating mutations in β-catenin concomitant with the activation of the Wnt signaling pathway and nuclear accumulation of β-catenin frequently occurs during gastrointestinal cancers, including colorectal cancer initiation and progression, and leads to an enhanced expression of diverse oncogenic products (Figures 1 and 2) [163-165].