For example, haematological malignancies driven by somatic PDGFRB mutations are very sensitive to Imatinib.24,25 Of note here, three separate population-based studies have identified a cis-acting protein quantitative trait locus (pQTL) located close to PDGFRB, influencing circulating levels of PDGFRB, that reaches genome-wide significance.26–28 If PDGFRB is an important target for Imatinib in PAH, common genetic variants influencing PDGFRB protein levels may affect therapeutic response, or at least the dose required to elicit a response, and the risk of dose-limiting adverse effects. The gene discussed is PDGFRB; the disease is pulmonary arterial hypertension.