Interestingly, two of these mechanisms (EZH2 amplification and miR-101 deletion) are encountered more frequently in advanced and castrate resistant prostate cancers than in primary untreated prostate cancers, and ETS family gene fusions and ERG protein overexpression are rarely seen in isolated PIN lesions or PIN lesions associated with ERG-negative carcinomas [34]. This evidence concerns the gene EZH2 and prostate carcinoma.