In the absence of Wnt ligands, β-catenin is phosphorylated and targeted for degradation, while Wnts bind to their receptors leading to its accumulation and translocation into the nucleus, where it combines with Tcf/Lef to stimulate the transcription of genes involved in the development and progression of cancer, such as COX-2, VEGF, survivin, c-Myc and cyclinD1 [52,53]. The gene discussed is PTGS2; the disease is cancer.