Our hypothesis is based on the phenomenon of recurrent infections experienced by the patient since childhood, triggering a chronic inflammatory response mediated by TNF-α, IL-1, and IL-6, which may predispose the liver, macrophages, and smooth muscle to maintain an inflammatory response that conditions the production of serum amyloid P (SAP) component and glycosaminoglycans (GAGs), precursors of amyloids that ultimately deposit in multiple organs [20]. The gene discussed is TNF; the disease is infection.