APC and colorectal neoplasm: Although APC mutations initiate the majority of human CRCs, a subset of human colorectal tumors with intact APC carries protein-stabilizing mutations in CTNNB1. For β-catenin ubiquitination and subsequent proteasomal degradation, the conserved N-terminal serine and threonine residues (S33, S37, T41, and S45) have to be phosphorylated.