Therefore the combined effects of dysregulation of dystroglycan function through proteolysis leading to altered cell adhesion and motility, changes in the scaffolding of MAPK signalling, nuclear translocation of dystroglycan coupled with increased ETV1 transcription, which also activates MAPK-dependent signalling that itself leads to an increase in cell migration, represents a positive feedback mechanism driving prostate cancer progression that warrants further investigation. This evidence concerns the gene ETV1 and prostate carcinoma.