These results have several important implications: first, β2AR agonism with formoterol had no effect on the morphology of mouse aorta; second, the beneficial effects of medium‐dose formoterol on AAA came into play only in the presence of EPO stimulation; and third, the null effect of high‐dose formoterol on AAA development cannot be explained by the direct harmful effect of high‐dose formoterol on mouse aortic tissues. The gene discussed is ADRB2; the disease is triple-A syndrome.