According to previous studies, the immune pathogenesis of SAA is that the mDCs are activated by some unknown antigens, express major histocompatibility complex (MHC) class II molecules, present antigens to help T cells (Th), induce the differentiation of Th0 to Th1, cause a Th1/Th2 imbalance, produce many type I lymphokines, and activate the CD8+ T cells, thus resulting in bone marrow failure. This evidence concerns the gene CD8A and Bone marrow hypocellularity.