The deletion site is characterised by two types of breakpoints, with the 3′ end of ERG consistently fused to the 5′ end of TMPRSS2. This fusion leads to the overexpression of ERG, facilitated by the androgen-responsive promoter of TMPRSS2, resulting in elevated PCa cell invasion, proliferation, angiogenesis, and tumour aggressiveness (39, 40). This evidence concerns the gene TMPRSS2 and posterior cortical atrophy.