At least eight of the other genes with case-derived de novo variants have plausible roles in lung/vascular development but have not been previously implicated in PAH: AMOT (angiomotin), CSNK2A2 (casein kinase 2 alpha 2), HNRNPF (heterogeneous nuclear ribonucleoprotein F), HSPA4 (heat shock protein family A member 4), KDM3B (lysine demethylase 3B), KEAP1 (kelch-like ECH-associated protein 1), MECOM (MDS1 and EVI1 complex locus), and ZMYM2 (zinc finger MIM-type containing 2). This evidence concerns the gene AMOT and pulmonary arterial hypertension.