The results showed that induced atherosclerosis was proportional to dietary intake of cholesterol because HC stress significantly activated specific proinflammatory pathways that is the platelet-derived growth factor (PDGF), interferon-γ (IFNγ), interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) signaling pathways. Here, TNF is linked to atherosclerosis.