Since extracellular HMGB1 is known to be able to interact with RAGE, and in turn participate to the cell activation, i.e., inducing proinflammatory phenotype (12), we investigated whether HMGB1 was secreted from monocytes treated with anti-β2-GPI antibodies from APS patients. This evidence concerns the gene HMGB1 and autoimmune polyendocrinopathy.