EHMT2 and cardiovascular disorder: Similarly, G9a is capable of H3K9me/me2 on the promoter of Beclin1 and P62 to transcriptionally inhibit autophagy flux, and then induces vascular smooth muscle cells death, indicating that G9a may be a potent therapeutic target for cardiovascular diseases including aortic dissection.56 In addition, Mtb phosphoribosyltransferase (MtbPRT) induces EHMT2-dependent H3K9me2/3 and reduces H3K9ac and H3K27ac by upregulating HDAC3 at the ATG5 and ATG7 promoter, which inhibit autophagy to promote Mtb survival57 (Fig. 2a).