Generally speaking, G9a may participate in carcinogenesis through either suppression of tumor suppressors, such as CDH1/E-Cadherin) [10] and p53 [11], or activation of oncogenic signaling pathways such as hypoxia-response [12] via transcriptional repression of a number of critical tumor suppressors or inhibitors in a histone or non-histone dependent manner in various human cancers [13, 14]. Here, EHMT2 is linked to neoplasm.