This will help us better understand underlying mechanisms of Ang II-induced VSMCs proliferation and inflammation, providing further basis for PRMT2 as a potential target against cardiovascular diseases associated with VSMCs proliferation and inflammation. In vivo research, however, is still needed to examine whether PRMT2 mediates VSMCs proliferation and inflammation and vascular remodeling in Ang II-induced hypertensive model. This evidence concerns the gene AGT and cardiovascular disorder.