Based on the findings [19, 22, 36] that inhibition of the reverse mode of NCX alleviated contrast-induced renal tubular cell apoptosis through suppressing the increase of intracellular Ca2+, ROS overproduction, p38 MAPK activation, and Caspase-3 overexpression and the findings [14, 37] that tail vein injection of inhibitor of reverse mode of NCX can exert protective effects on CI-AKI in rats through suppressing contrast-induced renal ET-1 overproduction and renal vasoconstriction, we propose the following hypothesis regarding the molecular mechanism of CI-AKI. The gene discussed is EDN1; the disease is acute kidney injury.