Of note, overexpression of HDAC2 could suppress the expression of arginase 2, a protein that counteracts eNOS activity, and the effect was reversed by TSA through increasing levels of H3K9 and H4K12 acetylation at arginase 2 proximal and core promoter (Pandey et al., 2014; Krause et al., 2016), indicating a protective role of HDAC2 in endothelial dysfunction and AS. The gene discussed is ARG2; the disease is endothelial dysfunction.