Since dosage of β-catenin is critical in determining epithelial cell fate in many organs and varying the level of β-catenin signaling during a cell fate program have been shown to switch the epithelial cell fate [40], it is possible that the homozygosity of Apc mutation (ApcΔ580/Δ580) results in too much β-catenin transcriptional activity, that may push cells into the signaling events that leads to squamous transdifferentiation rather than to hyperplasia of mammary epithelial cells and eventually to neoplasia. The gene discussed is APC; the disease is neoplasm.