These findings indicate that GLP/G9a play a key role in mediating SPOP mutation-induced DNA hypermethylation and proliferation in PCa cells and these effects are independent of the H3K9me2 methyltransferase activity, consistent with an HMTase-independent role of GLP/G9a in regulating DNA methylation reported previously24,43. This evidence concerns the gene EHMT1 and posterior cortical atrophy.