Deficiency or inhibition of neutral SMase2 lead to a reduction in atherosclerotic lesions, macrophage infiltration, and lipid deposition, as well as a reduction in IL-1β, IL-6, TNF-α and MCP-1 (monocyte chemoattractant protein-1) in Apolipoprotein E (ApoE)-null mouse models (used as a model of atherosclerosis) (Figure 2) (142). This evidence concerns the gene APOE and atherosclerosis.