Specifically, the loss of FTO upregulated endothelial prostaglandin D2 (PGD2) production via overexpression of its main synthase, lipocalin-type prostaglandin D synthase (L-PGDS), in resistance arteries, and thus alleviated specifically obesity-induced vascular dysfunction and hypertension but did not alter the baseline blood pressure.117. The gene discussed is FTO; the disease is obesity due to melanocortin 4 receptor deficiency.