Similarly, deletion of the region encompassing the risk-associated CTCF site on chr12 caused a ~ 100-fold increase in expression of KRT78; in this case, four of the other nearby KRT genes also showed increased expression, albeit not as high as KRT78. The very large increases in gene expression that we observed upon deletion of regions encompassing PCa risk-associated CTCF sites are interesting due to the fact that removal of CTCF or the cohesin component RAD21 from the cell has quite modest overall effects on the transcriptome. The gene discussed is KRT78; the disease is posterior cortical atrophy.