Although both the ETS transgenic overexpression models and our Tmprss2-ETS knockin models suggest that ectopic expression of ERG or ETV1 alone in murine prostates is not sufficient to initiate prostate tumorigenesis, mouse modeling studies further demonstrated that ectopic ERG or ETV1 expression can cooperate with Pten-loss (thus leading to activation of the PI3K pathway) to drive prostate cancer development [8–10]. This evidence concerns the gene PTEN and Familial prostate cancer.