Rather, alternative explanations for the canonical pathway activation have been proposed for mammary tumors, including (1) mutations in other components of the pathway, (2) overexpression of Wnt ligands and other activators, (3) loss or downregulation of the antagonists, such as sFRP1, and (4) cross regulation by other deregulated pathways, such as epidermal growth factor (EGF), phosphatase and tensin homolog (PTEN), or tumor protein 53 (p53) signaling (117, 118). This evidence concerns the gene TP53 and breast cancer.