We have identified PCa risk-associated CTCF anchor regions that appear to function by creating a repressive regulatory environment; deletion of these anchor regions results in a very large increase (~ 100-fold) in expression of KCNN3 (upon deletion of the CTCF site on chr1) or KRT78 (upon deletion of the CTCF site on chr12). This evidence concerns the gene KCNN3 and posterior cortical atrophy.