Such small molecule, approved for the treatment of the pulmonary arterial hypertension and known for its well-tolerated toxicity profile [52–54], and able to block simultaneously HG-SOC cell functions mediated by ETAR, and the tumour-supportive activity of stromal components expressing ETBR [14], may represent a very promising candidate for drug repurposing in HG-SOC patients, even in the setting of advanced and resistant forms of the disease. The gene discussed is EDNRA; the disease is pulmonary arterial hypertension.