Our findings of VSMC senescence in EPO‐induced AAA are consistent with our previous report of vascular inflammation and collagen degradation by EPO injection in mice.[17] Moreover, we found that medium‐dose formoterol upregulated SIRT1 expression and protected mouse aortas from AAA, which agrees with a previous report that overexpression of SIRT1 in VSMCs of ApoE−/− mice suppressed VSMC senescence and AAA formation.[4] Taken together, medium‐dose formoterol may reverse the aging process in EPO‐induced AAA via SIRT1 upregulation. The gene discussed is APOE; the disease is triple-A syndrome.