Aged ECs generate excess reactive oxygen species (ROS) through mitochondrial respiratory chain, NADPH oxidases and down regulation of antioxidant enzymes (Donato et al., 2015) to create chronic oxidative stress and subsequent low-grade inflammatory phenotype in the aortic wall (Ungvari et al., 2008), which leads to severe aortic pathologies such as atherosclerosis and abdominal aneurysm (AAA) (Ungvari et al., 2010; Peshkova et al., 2016; Golledge, 2019) in aged people. Here, FMO5 is linked to triple-A syndrome.