Colorectal cancer is the second most common cause of cancer mortality in the western world. Colorectal cancer has been well studied, and the genetic steps involved in the adenoma to carcinoma sequence have been well elucidated. The first genetic alteration, found in 85% of adenomas, are mutations in the adenomatous polyposis coli (APC) gene. However, the consequences of this and the exact function of APC in the colon is not fully understood. It has been suggested that APC could function through its regulation of beta-catenin, an ubiquitous cytoskeletal protein with multiple binding specificities resulting in diverse functions including cell growth, adhesion, and migration. Any change in these associations may play a role in colorectal cancer development and progression.