In ITP pathogenesis, the interaction between BAFF and its receptor (BAFF‐R) not only diminishes apoptosis rates in B cells and CD8+ T lymphocytes via induction of anti‐apoptotic proteins BCL‐2 and BCL‐xl, but also facilitates B‐cell proliferation, accelerates regulatory T cell (Treg) apoptosis, and enhances differentiation and expansion of Th17 cells [35, 36]. This evidence concerns the gene TNFSF13B and autoimmune thrombocytopenic purpura.