Irrespective of the serum concentrations of all lipoprotein fractions and subfractions in P-407-treated mice relative to control mice, it is extremely important to emphasize that despite the presence of antiatherogenic HDL3, and especially HDL2, the capacity for the atherogenic lipoprotein fractions and subfractions to induce the formation of aortic atherosclerotic lesions in P-407-treated mice is not completely inhibited by HLD2 and HDL3, since this is a well-established mouse model of hyperlipidemia and atherogenesis [6, 13, 18, 19]. Here, GJC2 is linked to hyperlipidemia.