Finally, it has been reported that the inhibition of FAK in vitro and in vivo decreased self-renewal capacity, by decreasing the levels of Wnt3a and β-Catenin, thus demonstrating a novel FAK-Wnt axis regulating BCSC activity and indicating the FAK-Wnt axis as promising target to eradicate self-renewal capacity and progression of human breast cancers [15]. This evidence concerns the gene PTK2 and breast carcinoma.