When docked, the <i>TLR9-TLR9</i> dimer and <i>FAS-FASGL</i> models, redistributed interfacial contacts, potentially reducing binding efficiency, whereas docked <i>TNFRSF1B-TRAF2</i> interactions were partially maintained.<h4>Conclusion</h4>These findings suggest that MD distinct immune phenotypes based on systemic inflammation and may be linked to comorbid autoimmune/autoinflammatory disorders, with rare variants in <i>TLR9</i>, <i>TNFRSF1B</i> and <i>FAS</i> likely contributing to autoinflammation. The gene discussed is TNFRSF1B; the disease is Autoimmunity.