The model proposes that a majority of individuals diagnosed as Chronic Illnesses, based on clinical criteria, may be potentially defined as AntiPhospholipid Antibody Syndrome (APS) with the endothelial cell (EC) as the disease target. These patients have a hypercoagulable state demonstrated by increased markers of coagulation activation and increased blood viscosity due to the generation of Soluble Fibrin Monomer (SFM). 

The CFS / FM process may be triggered by a variety of pathogens (CMV, HHV6, Mycoplasma, Chl. pneumonia, etc.), resulting in pathogen-mediated immune activation that induces antibodies which cross react with endothelial cell (EC) protective proteins B2GPI & Annexin V. These antibodies dislodge the protective proteins from endothelial cell (EC) surfaces, exposing PhosphatidylSerine (PS) on the endothelial cell (EC) surfaces in capillary beds. Pathogens induce inflammatory responses which include cytokine modulation of endothelial cell (EC) to down regulate the antithrombotic environment (Thrombomodulin, tPA) in favor of prothrombotic expression of Tissue Factor (TF). TF and PS exposure allows binding of the coagulation tenase and prothombinase complexes to endothelial cell (EC) surfaces. This results in thrombin generation leading to SFM formation. SFM dimerizes easily, increasing blood viscosity and precipitating out on endothelial cell (EC) surfaces as fibrin(oid) deposition, creating local ischemia and pathology, blocking nutrient and oxygen delivery in the microcirculation.