Binding to TLR2 activates platelets by enhancing phosphatidylinositol 3-kinase (PI3K) signalling [34], while binding to TLR4 triggers the activation of the NF-κB and MAPK pathways, leading to inflammatory responses that contribute to APS-related thrombosis [35]. Here, NFKB1 is linked to autoimmune polyendocrinopathy.