Conversely, the exposure of endothelial cells to aPL upregulates endothelial expression of monocyte chemoattractant protein 1 (MCP-1), which in turn promotes TF synthesis by monocytes (Figure 1A) (Cho et al., 2002), leading to thrombotic complications in patients with primary APS (Cuadrado et al., 1997). The gene discussed is CCL2; the disease is autoimmune polyendocrinopathy.