These findings may be explained by the side effects of vasopressin: (1) vasopressin causes coronary vasoconstriction with decreased coronary blood flow and weaker cardiac contractility [57, 58], (2) vasopressin leads to systemic vasoconstriction with increased cardiac afterload and higher risk of cardiac pathology [58–60], and (3) vasopressin may participate in cardiac inflammation and fibrosis by promoting IL-1β expression through the β-arrestin2-mediated NF-κB signaling pathway in humans [61]. The gene discussed is NFKB1; the disease is inflammation.