Intense increase in AnxA1 gene activity and protein synthesis in hepatocytes, endothelial cells, and leukocytes at the beginning of the inflammatory process, followed by reduction in AnxA1 expression in the late phase of inflammation, was verified by means of the LacZ reporter gene in AnxA1-null mice after LPS endotoxemia [61]. Here, ANXA1 is linked to serum lipopolysaccharide activity.