The hypothesis tested in the present study was that open AAA repair (OR) and/or endovascular AAA repair (EVAR) possibly affect in a different way OPN or OPG serum levels, since (a) increased OPN and OPG values have been associated with the development and growth of AAAs [13–15] and (b) OR and EVAR affect differently the aneurysmal tissue exclusion from systemic arterial circulation. The gene discussed is TNFRSF11B; the disease is triple-A syndrome.