Most colorectal carcinomas develop from adenomas via adenoma-carcinoma-sequence driven by the accumulation of genetic and epigenetic mutations (Fearon and Vogelstein, 1990); Our results (Figure 5) imply that FAK/PYK2/GSK3βY216/β-catenin regulation axis is an early participant and driving force for intestinal tumorigenesis in APCmin/+ mice. This evidence concerns the gene PTK2 and colorectal carcinoma.