NLRX1, NOD-like receptors family member X1, is significantly downregulated following intestinal MI/R injury [35], and ablation of the mitochondrial NLRX1 exerts a detrimental effect on acute cardiac infarction induced by a prolonged ischemia-reperfusion episode and activates potential MI/R injury mechanisms contributing to increased MI/R injury, related to elevated energy metabolism and diminished Akt [36]. The gene discussed is AKT1; the disease is myocardial infarction.