In most cases, Wnt/β-catenin pathway is activated by a mutation in APC tumor-suppressor; in many remaining cases, mutations in β-catenin itself at sites of GSK3β phosphorylation lead to β-catenin cytoplasmic accumulation and activation as transcription factor to induce the expression of several target genes, including c-myc, cyclin D1, uPAR, c-jun, and fra-1 [14-17], involved in cell growth. The gene discussed is APC; the disease is neoplasm.