Further functional studies of TMPRSS2-ERG have shown modest evidence of oncogenic activity with cooperating transforming events [27, 28]: TMPRSS2-ERG fusion as the single most established PCa molecular lesion [27], meaning expression of N-terminally truncated ERG protein under control of TMPRSS2 androgen-responsive promoter [38]. The gene discussed is TMPRSS2; the disease is posterior cortical atrophy.