Although mitochondrial oxidative stress is a prevalent root cause for metabolic diseases, reliance on the antioxidation strategy (e.g., ROS scavenging or SOD mimicry) is inadequate for addressing disease‐specific pathological issues.[275] For instance, in NAFLD, the contradictory mechanisms of compensatory enhancement of mitochondrial β‐oxidation and lipid toxicity‐induced ROS bursts suggest that combined regulation of lipid metabolism by nanomedicines should be implemented. This evidence concerns the gene SOD1 and metabolic disease.