In agreement with these results, it has been observed that the genetic disruption of CB2 in Apolipoprotein E-deficient mice (ApoE−/−), a murine model of atherosclerosis, is the cause of boosted O2•− generation, whereas its stimulation reduced vascular O2•− release, resulting in the suppression of ROS/RNS generation and a subsequent reduction in the size of atherosclerotic lesions (Figure 5) [200]. The gene discussed is APOE; the disease is atherosclerosis.