The activities of complexes I and II of the mitochondrial respiratory chain were diminished in the hearts from animals with sepsis (Piel et al., 2007; Neviere et al., 2016), and this might be due to the detrimental effects of sepsis mediators such as NO, TNF-α, IL-1β, etc. In addition, ROS accumulation can suppress mitochondrial function by destroying mitochondrial proteins, lipids, and DNA through structural modifications during sepsis in a positive feedback fashion as failed mitochondria led to significantly slower ROS scavenging (Potz et al., 2016). The gene discussed is IL1B; the disease is Sepsis.