And one of the senescence biomarkers was phosphorylation of Histon H2AX at serine139, known as γH2AX, which derived from DNA double‐strand breaks. In an attempt to reveal the role of senescence in both EPO‐induced AAA and the effect of formoterol on EPO‐induced AAA, we examined the number of γH2AX foci in the aortic tissues in vehicle, EPO, and EPO + medium‐dose formoterol groups. The gene discussed is H2AX; the disease is triple-A syndrome.