To look for epigenetic changes in primary GBMs that could affect JMJD3 expression and function, whole genome DNA methylation arrays were performed on a series of parental glioblastoma samples (GBM-P, n = 7) which demonstrated that compared to non-tumor brain tissue, all GBM samples show relative hypermethylation of a CpG site (Illumina cg09911083) within the JMJD3 intragenic regulatory element (Figure 6A; Chr.17p13.1∶7,695,644–7,696,309; UCSC NCBI36/Hg18[30]–[32]). This evidence concerns the gene KDM6B and neoplasm.