Our findings indicate that RBCs isolated from ApoE/LDLR−/− mice released higher amounts of ATP in response to hypoxia, compared to their age-matched controls, what could be linked to an increase in the expression of Gi protein on RBC membranes, which was reported in RBCs of humans with atherosclerosis (Kots et al., 1993). This evidence concerns the gene LDLR and atherosclerosis.