Endothelial dysfunction, which was manifested in the form of diminished NO bioavailability, was well compensated for by an increased expression of KCa3.1 protein, as shown in aged wild‐type, CerS2 null, and catalase−/−/GPX1−/− mice, and an upregulation of KCa3.1 channel activity. The gene discussed is CERS2; the disease is endothelial dysfunction.