A novel approach for developing therapy for APS has shown that tolerogenic dendritic cells specific for domain-I of the β2GPI molecule may have potential in attenuating experimental APS in a murine model, via acceleration of the differentiation of CD4+ T cells to Treg cells, decreased proinflammatory cytokine production, and increased anti-inflammatory cytokine expression (IL-10 and TGFβ)25. This evidence concerns the gene CD4 and autoimmune polyendocrinopathy.