Although concrete data are currently insufficient to firmly establish an epigenetic role of AM in PAH, recent findings highlight that altered DNA methylation levels at specific gene loci such as superoxide dismutase 2 and granulysin, variations in histone H1 levels, aberrant expression of HDACs and bromodomain-containing protein 4, and disruptions in microRNA networks contribute to the emerging role of epigenetics in PAH [58,163]. Here, GNLY is linked to pulmonary arterial hypertension.