We first evaluated the impact of prolonged hypercholesterolemia on Cx36 expression in vivo using the hypercholesterolemic, pro-atherogenic ApoE deficient mouse (ApoE−/−) [22], [23], [24] and observed that the Cx36 levels were decreased in ApoE−/− compared to WT mice. This evidence concerns the gene APOE and familial hypercholesterolemia.