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). The gene discussed is KRT78; the disease is posterior cortical atrophy.