APC and colorectal carcinoma: Furthermore, β-catenin signaling can also be mediated by Wnt-independent signaling, such as EGFR [4], AKT [5] and JNK [6] etc. Although it has been reported that more than 80% of CRC have APC truncation/mutation or β-catenin mutation, both of which can activate the Wnt/β-catenin signaling during colorectal cancer development [7–9], Wnt/β-catenin signaling is also modulated through various other mechanisms in cancer, including crosstalk with other altered signaling pathways [7].