On the other hand, DKO mice failed to show elevated LPL in the adipose tissue relative to Par-4+/+ mice and failed to induce fat storage despite the lack of Par-4, implying that C3/ASP that was elevated in response to Par-4 loss was an essential downstream mediator of adipocyte hypertrophy, fat storage and obesity in Par-4 knockout mice. This evidence concerns the gene LPL and obesity disorder.