The increase reported here in the procoagulant activity on the endothelial cell surface mediated by IgG APS, particularly observed in the APSNR group, could be linked to these previously reported APS-related mechanisms, including TF overexpression, reduced thrombomodulin expression, and decreased nitric oxide (NO) release (15, 17, 37). The gene discussed is TF; the disease is autoimmune polyendocrinopathy.