We performed ChIP-Seq profiling of three active histone marks (H3K27ac, H3K4me1, H3K4me3) and RNA-Seq in small pulmonary artery endothelial cells (PAECs) harvested from individuals suffering from either hereditary PAH (HPAH; carrying a BMPR2 mutation; n = 2) or idiopathic PAH (IPAH; no known mutation; n = 8) along with control subjects (n = 9; Fig. 1a, Supplementary Fig. 1a, b; Supplementary Data 1). This evidence concerns the gene BMPR2 and heritable pulmonary arterial hypertension.