They found that the loss of Sema4D expression ameliorates the effects of dyslipidemia on the platelet function in vivo and ex vivo, and reduces atherosclerotic lesions in hyperlipidemic mice on a high-fat, high-cholesterol diet for 3 or 6 months (Zhu et al., 2009) (Figure 4A). This evidence concerns the gene SEMA4D and metabolic syndrome.