However, our previous study found that in ApoE−/− mice, EPOR knockdown decreased the incidence of AAA in AngII model, indicating that EPO/EPOR signaling is essential for AngII‐induced AAA.[17] Thus, it is likely that formoterol treatment may also benefit AngII‐induced AAA albeit further experiment is needed for confirmation. This evidence concerns the gene APOE and triple-A syndrome.