Given the fact that AMPK activity (indicated by phosphorylation of AMPKα) decreased in macrophages upon pro-inflammatory stimulus (LPS) in vitro, and in joints during the peak of inflammatory arthritis in vivo, and the ability of A-769662 to prevent inhibition of inflammatory responses, AMPK could be a promising pharmacologic target in arthritis [24]. This evidence concerns the gene PRKAA1 and Arthritis.