For example, studies by Cañes et al. (2021) showed that overexpression of human NOR1 in the vasculature of mice, particularly in VSMCs, enhances Ang II-induced production of proinflammatory cytokines, chemokines, and reactive oxygen species, Ang II-induced increase in matrix metalloproteinase activity, and Ang II-induced disruption of elastin integrity in vascular tissue, which subsequently increases the occurrence and severity of AAA (Table 1). Here, NR4A3 is linked to triple-A syndrome.