Mechanistically, it is unlikely that G9a inhibition directly results in the abolition of ER stress, as the level of H3K9me3, the chromatin repressive mark to which G9a contributes, is reduced on the promoters of Chop and BiP/Grp78 genes concomitant with their upregulation during ethanol-induced chronic liver injury and ER stress in mice [40]. This evidence concerns the gene DDIT3 and Endoplasmic Reticulum Stress.