Although Akt1 is a well-known mediator of oncogenic transformation15 and prostate tumour growth,6, 8 our current study demonstrates for the first time that endothelial-specific Akt1 loss will promote prostate cancer metastasis via nuclear translocation of β-catenin and suppression of endothelial tight-junction protein expression. The gene discussed is AKT1; the disease is prostate carcinoma.