We propose that the pathogenesis of AA may involve abnormal autoimmune CD8+ T lymphocytes produced by thymomas bypassing the selection process in the thymic medulla and migrating to peripheral tissues [4,6,14], leading to the loss of immune privilege of hair follicles, the upregulation of inflammatory pathways, and autoimmune-mediated follicular destruction [8,9,15,16]. The gene discussed is CD8A; the disease is thymoma.