According to Richter et al.8, FGF23 and its co-receptor Klotho dysregulations were associated with endothelial dysfunction in humans, but in vitro experiments were performed to assess the effects of FGF23 in relation to its co-receptor Klotho on nitric oxide (NO) synthesis and ROS formation via activation of NADPH oxidase 2. The gene discussed is KL; the disease is endothelial dysfunction.