In prostate cancer cells, the effect of GSK-3 on β-catenin phosphorylation is also dependent on Src-mediated phosphorylation of its tyrosine 218 residues.18, 19 On the other end, reduced Akt1 activity in endothelial cells is associated with increased Src activity.21 In our study, shAkt1 HLECs exhibited increased GSK-3 tyrosine 218 phosphorylation, increased β-catenin phosphorylation, and its nuclear translocation compared to shControl cells indicating the role of GSK-3 in the process. The gene discussed is AKT1; the disease is Familial prostate cancer.