SAA1 and Fabry disease: Concurrently, dysregulation of FCN2 – a key soluble pattern recognition molecule in the lectin complement pathway – potentiates local inflammation by impairing microbial clearance, positioning FCN2 as a critical contributor to FD pathogenesis.[28] SAA1, an acute-phase reactant predominantly synthesized by hepatocytes, exhibits a positive correlation with disease activity in inflammatory bowel disease.