Addition of rHB-EGF attenuated the elevated levels of intracellular ROS, O2−, and MDA elicited by H2O2 and restored stromal cell differentiation, demonstrating an antioxidant function of HB-EGF in oxidative stress, which was further reinforced by the observation that HB-EGF might decrease the production of intestinal ROS in the ischemia/reperfusion injury model [12]. The gene discussed is EGF; the disease is ischemia.