The current study clearly show that by phosphorylating GSK3α/βY279/Y216, FAK and PYK2 function redundantly in the regulation of Wnt/β-catenin signaling in CRC cells, raising the possibility that FAK and PYK2 could also function redundantly in Wnt-driven intestinal tumorigenesis. This evidence concerns the gene GSK3A and colorectal carcinoma.