Senescent VSMCs have been reported to accumulate in atherosclerotic plaques in mice and humans.34,35 Our previous study demonstrated a causal role for senescent VSMCs in the development of mouse AAAs.13 In this study, we provided evidence that cellular senescence occurs in human TAAs and is correlated with the expression of the vascular inflammation orchestrator IL-1β. The gene discussed is IL1B; the disease is achalasia-alacrima syndrome.