It is important to emphasize that the majority of TLR4 involvement in APS activity is inferred from downstream signaling changes, antibody-blocking experiments, and receptor-expression modulation; direct biophysical confirmation of APS–TLR4/MD-2 binding (e.g., SPR, ITC) remains limited to date. The gene discussed is TLR4; the disease is autoimmune polyendocrinopathy.