These results demonstrate that the increased expression of KCNN3 and KRT78 is not simply a response to the method of CRISPR-mediated deletion but rather suggest that the regions encompassing the PCa risk-associated CTCF sites are more important in regulating the expression of these genes than are the CTCF sites at the other end of the loops. Here, KCNN3 is linked to posterior cortical atrophy.