HNF1B and posterior cortical atrophy: Our findings demonstrated not only multiple potential causal SNPs and risk CREs within 17q12/HNF1B locus, and the responsibility of TMPRSS2-ERG fusion for transforming molecular and biological effects of 17q12 and regulating HNF1B expression, but also mapped genome-wide binding sites of HNF1B and defined its high rate of chromatin co-occupancy with TMPRSS2-ERG that can explain more of genetic associations discovered by GWASs in PCa.