The aims of this study were (1) to assess and quantify the effect of the functional IL6R variant on the progression of AAAs in population cohorts with prospective follow-up and standardized repeated measurements of AAA diameter and (2) to estimate the effect of blocking the IL-6 signaling pathway (ie, either both classical and trans-signaling pathways or specifically the trans-signaling pathway) on time to aneurysm rupture in mouse models. The gene discussed is IL6R; the disease is triple-A syndrome.