Several studies addressing the effects of IFN-α on EC of different origin have shown that IFN-α inhibited the endothelial repair, reduced the transcription of endothelial nitric oxide synthase (eNOS), reduced the eNOS cofactor availability, and increased reactive oxygen production, which may collectively lead to endothelial dysfunction [44–46]. The gene discussed is NOS3; the disease is endothelial dysfunction.