It has been well known that β2AR desensitization occurs when β2AR is exposed to excessive agonists.[47] The mechanism involves the uncoupling of β2AR from adenylate cyclase and the internalization of β2AR.[11] In this study, the null effect of high‐dose formoterol on EPO‐induced AAA may be related to β2AR internalization. This evidence concerns the gene ADRB2 and triple-A syndrome.