The depletion of Vδ2 T‐cells and increased cytotoxicity are unique features in AA, consistent with acquired chronic pure red cell aplasia.[30] FASLG expression is upregulated in CD8+ T‐cells during cell activation.[31] FASLG inhibits normal hematopoiesis in myelodysplastic syndrome marrow.[32] Our results support the notion that FAS‐FALG signaling is a therapeutic target for AA. Here, CD8A is linked to myelodysplastic syndrome.