Our results from integrative bioinformatic analyses provide convincing evidence for a decisive role of the DNA methylation status of IRAK1-DMR in transcriptional activation of IRAK1. These findings were further supported by our in vitro cell culture experiments, showing in the PCa cell line DU145 that weak endogenous IRAK1-mRNA expression is correlated with hypermethylation of IRAK1-DMR and can be dramatically increased (>400%) by combined treatment with the DNMT1 inhibitor 5-AZA and the HDAC inhibitor TSA. Here, HDAC9 is linked to posterior cortical atrophy.