In response to the Wnt signal, β-catenin accumulates in the cytoplasm and is translocated to the nucleus, where it binds to T-cell factor (TCF)/lymphoid enhancer factor transcription factors and regulates the expression of target genes involved in the proliferation and invasiveness of cancer cells and angiogenesis.3, 4 Loss-of-function mutations in APC or mutations in β-catenin at the phosphorylation site, which are found in almost all human colorectal cancers, lead to stabilization of the β-catenin protein and aberrant activation of Wnt/β-catenin signaling. Here, APC is linked to colorectal cancer.