TNFRSF12A and metabolic disease: There is little information available on the behaviour of TWEAK and its mechanism of action in the context of atherosclerotic inflammation and metabolic disease in various cells; however, it could be speculated that increases in CD163 act to counteract increased Fn14 expression and competitively bind to TWEAK to simultaneously encourage potential beneficial CD163-TWEAK interactions and negate negative Fn14-TWEAK interactions.