CCL2 and hyperlipidemia: Consistently, AAV8-ApoL1 G2 treated hamsters exhibited more atherosclerotic lesions in both whole aortas and aortic roots with more CD68 and MCP1 (monocyte chemoattractant protein 1), but less αSMA (alpha-smooth muscle actin) expression when compared with other two groups, suggesting that ApoL1 G2 could enhance local vascular inflammation to contribute to atherosclerotic development in a plasma lipid-independent manner in the setting of hyperlipidemia (Fig. 1F).