In contrast to SKA-31 treatment, daily administration of the KCa3.1 channel blocker senicapoc (40 mg/kg) did not mitigate endothelial dysfunction in abdominal aortic rings compared with vehicle treated Apoe−/− HFD mice (Figure 2), nor did it modify SNP-mediated relaxation (Figure 4), or PE-induced smooth muscle contraction (Figure 6). This evidence concerns the gene APOE and endothelial dysfunction.