FOXRED1, as a key accessory factor of mitochondrial complex I, is crucial for maintaining mitochondrial functional homeostasis.[28] Previous studies have established that metabolic disorders in mitochondrial Complex I play a critical role in promoting malignant tumor progression by activating the mTOR pathway.[40, 41] Subsequently, we demonstrated that knocking down FOXRED1 promoted the activation of the mTOR/c‐MYC pathway by downregulating the expression of mitochondrial Complex I subunits (NDUFS2, NDUFB9) (Figure S14D,E, Supporting Information). This evidence concerns the gene NDUFS2 and metabolic disease.