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. This evidence concerns the gene TNK2 and Familial prostate cancer.