SAA1 (serum amyloid A1) is a major acute-phase protein synthesized predominantly by hepatocytes that functions as a key mediator of innate immunity and inflammation 1. As a lipophilic protein, SAA1 contributes to HDL and cholesterol transport while interacting with specific receptors including TLR4 to modulate immune responses 1. Mechanistically, SAA1 promotes pathogenic Th17 cell differentiation through direct T cell signaling in collaboration with STAT3-activating cytokines, and activates NF-κB signaling via TLR4/MD2 binding, triggering a feedforward inflammatory circuit 23. SAA1+ fibroblasts regulate macrophage infiltration and M1 polarization through chemokine secretion, supporting periodontal inflammation progression 4. Clinically, SAA1 elevation is associated with multiple inflammatory diseases: it exacerbates nonalcoholic fatty liver disease (NAFLD) through hepatic inflammation 3, contributes to colitis-related Th17 responses 5, and appears upregulated in psoriasis and atopic dermatitis sebaceous glands 6. Pathologically, SAA1 fragments can form insoluble amyloid fibrils causing secondary amyloidosis with renal manifestations in chr11 inflammatory disorders 7. These findings position SAA1 as a therapeutic target for inflammatory and metabolic diseases, with potential benefits from anti-SAA1 interventions in NAFLD, colitis, and periodontitis.