Eva NG et al. (2016) reported that HDAC3 regulates SOD3 expression in hPASMCs from patients with IPAH, where HDAC3 knockdown, but not HDAC1 or HDAC2, inhibited cell proliferation and upregulated SOD3 expression, supporting its therapeutic potential [9]. This evidence concerns the gene SOD3 and idiopathic pulmonary arterial hypertension.