It has been previously reported that the in vitro and in vivo inhibition of FAK decreased self-renewal capacity, by decreasing the levels of Wnt3a and β-Catenin, thus demonstrating a novel FAK-Wnt axis regulating breast cancer stem cell activity and indicating the FAK-Wnt axis as promising target to eradicate self-renewal capacity and progression of human breast cancers [15]. The gene discussed is WNT3A; the disease is breast carcinoma.