NDUFS4 and Leigh syndrome: In that study, Johnson and colleagues demonstrated that chronic administration of a high dose of rapamycin, a compound that inhibits a protein kinase called mechanistic target of rapamycin complex 1 (mTORC1), delays the onset and progression of neurological symptoms in a mouse model of Leigh syndrome and mitochondrial complex I deficiency due to the lack of the Ndufs4 subunit of the mitochondrial complex I [1].