While these and numerous other factors have been reported in AA over the decades (31), the classical features of active disease include the brisk infiltration of immune cells in a classic ‘Swarm of Bees’-like pattern (32), and the production of autoantibodies to HF-associated proteins (33–35). Recently, in an interesting transcriptomics study, Borcherding et al., observed clonal expansions of both CD4+ and CD8+ T cells, with shared clonotypes across varied transcriptional states in murine and human AA, suggesting autoantigen-dependent cellular autoimmune response in AA (36). This evidence concerns the gene CD8A and hydrops fetalis.