Although the role of the inflammatory environment in the increase in TFH frequency could not be completely excluded, Audia et al. (2) strongly suggested that the expansion of TFHs could be involved in B-cell recruitment and differentiation in the spleen of ITP patients, through IL-21 secretion and by the interaction of CD154 with CD40, contributing to the development of plasma cells producing antiplatelet autoantibodies. The gene discussed is IL21; the disease is autoimmune thrombocytopenic purpura.