In contrast, higher doses (≈8 mg kg−1) of rapamycin application in a Ndufs4 knockout mouse model of Leigh syndrome mitigated mitochondrial disease symptoms without affecting mitochondrial complex expression.[57] Moreover, doses exceeding 8 mg kg−1 were found to be more beneficial for health and survival in the Ndufs4 knockout model.[58] Therefore, the dose‐dependent effects of rapamycin on various disease models warrant further detailed investigation. Here, NDUFS4 is linked to inborn mitochondrial metabolism disorder.