The majority of breast tumors exhibit evidence of activation of canonical Wnt/β-catenin signaling and alterations predicted to upregulate Wnt/β-catenin signaling have been reported, including epigenetic silencing of Wnt antagonists SFRP1 and WIF1 and upregulation of Wnt ligands and Fzd receptors [7], [8], [33]. The gene discussed is WIF1; the disease is breast neoplasm.