Not surprisingly, ACK1 activation resulted in a significant decrease in the deposition of dimethyl H3K9 epigenetic marks, while its inhibition restored the repressive marks and caused transcriptional suppression of the ER-regulated genes such as the mammary tumor oncogene, HOXA1. Although AR is known to interact with KDM3A (143,144), whether ACK1/AR signaling utilizes KDM3A to erase the repressive H3K9 methylation marks to activate ATM expression to promote radioresistance of castration resistant prostate cancer is unknown. The gene discussed is ATM; the disease is prostate cancer.