Supporting this hypothesis, PTEN deletion is more common in prostate tumors with TMPRSS2-ERG rearrangements, than in those without [16,20], and in mouse models, ERG over-expression results in adenocarcinoma only when accompanied by a second mutation that activates the PI3K/AKT pathway [16,20,21]. The gene discussed is AKT1; the disease is prostate neoplasm.