Therefore, an impairment of SirT1 activity by oxidative post-translational modifications may be causally linked to the development of AA, at least in individuals with Marfan’s syndrome, possibly by exacerbating the deleterious effects of oxidant stress, whereas preventing or boosting SirT1 activity in the aortic wall may prevent AA. The gene discussed is SIRT1; the disease is Marfan syndrome.