Once in the liver, fatty acids from chylomicron remnant absorption may directly contribute to pathogenesis and cholesterol will induce triglyceride and fatty acid production through LXR responsive genes [50]–[52] Our data demonstrating steatosis without inflammation in Ccr2−/− and Cd44−/− mice are likely the result of the lipid source being directly related to dietary absorption thereby negating the role of the immune system on hepatic lipid accumulation. Here, CD44 is linked to steatosis.