TF and autoimmune polyendocrinopathy: Inflammatory, immunological, and thrombotic abnormalities, from which the clinical manifestations of SLE–APS originate, include activation of different cell types, such as endothelial cells (ECs), monocytes, and platelets; activation of the complement system; activation of the coagulation cascade and inhibition of fibrinolysis pathways; increased expression of tissue factor (TF); and impaired function of annexin A5 [12,25].