Then, the suppression of the activity of (3’-phosphoinositide-dependent kinase 1)-PDK1/Akt/Bad signaling was demonstrated underlying n-3 PUFA-induced apoptosis in prostate cancer (PC3, LNCaP and DU145) cells in vitro and in vivo; moreover, the suppression was dependent on the upregulation of SDC-1, and 15-LOX-1-mediated metabolism of DHA was required for SDC-1 upregulation [64]. The gene discussed is AKT1; the disease is prostate carcinoma.