Additionally, Bose [32] showed that recurrent point mutations and focal deletions of ERF cause decreased protein stability, and most occur in tumors without ERG upregulation; they argue that the oncogenicity of ERG is mediated, in part, by competition with ERF, and that overexpression of ERF blocks ERG-dependent tumor growth, and loss of ERF rescues TMPRSS2-ERG-positive prostate cancer cells from ERG dependency. This evidence concerns the gene ERG and prostate carcinoma.