We have recently reported that β-catenin is physically associated and activated by pp60(c-Src) kinase and is constitutively phosphorylated on the tyrosine residue in human colorectal and breast cancer cells [24, 27]; therefore, Src activation converts β-catenin's role from a cell-cell adhesion molecule to a transcriptional regulator via its interaction with the Tcf/Lef family of transcription factors [47, 48]. The gene discussed is HNF4A; the disease is breast carcinoma.