First, 121 genes were involved in the formation of AAA induced by EPO; Second, formoterol was predicted to be able to create gene expression patterns opposite to effects of EPO on aortas; Third, formoterol exhibited a dose‐dependent and U‐shaped effect on EPO‐induced AAA, and formoterol at a medium dose remarkedly reduced the incidence of EPO‐induced AAA, dilation of abdominal aortas and mortality of mice with AAA; Fourth, medium‐dose formoterol attenuated VSMC senescence induced by EPO via β2AR and subsequent activation of cAMP. The gene discussed is EPO; the disease is triple-A syndrome.