With respect to the interaction between ROS and EDH, as mentioned in the preceding text, ROS may impair EDH-mediated responses in several ways (e.g., the inhibition of intracellular Ca2+ mobilization, the oxidation of LDL, the disruption of caveolae, and the inhibition of function and/or expression of the KCa channel) in vascular endothelial cells of animal models of diabetes. This evidence concerns the gene GJB6 and diabetes mellitus.