Dysfunctions of KCa2.3 and KCa3.1 that are associated with membrane hyperpolarization and EDH-mediated dilation are implicated in cardiovascular pathologies, including diabetes, atherosclerosis, inflammation, cancer, and fibrosis (Grgic et al., 2009; Kohler et al., 2016). This evidence concerns the gene KCNN4 and atherosclerosis.