Treatment with EPO monoclonal antibodies andEPO receptor (EPOR) gene knockdown (Epor+⁣/-Apoe-⁣/-) significantlyreduced the incidence of AAA in an Ang II-induced mouse model [83].Mechanistically, EPO induced endothelial migration, proliferation, and tubeformation through the JAK2/STAT5 signaling pathway in vitro andex vivo experiments [83]. The gene discussed is APOE; the disease is triple-A syndrome.