Knocking down ATF4 downstream targets serine hydroxymethyltransferase 2 (Shmt2) and mitochondrial NAD-dependent methylenetetrahydrofolate dehydrogenase-cyclohydrolase (Nmdmc) leads to mitochondrial fragmentation and loss of ΔΨm, and suppressing the upregulation of these targets in the same PD fly models worsened their phenotype, while overexpression of these targets improved the model phenotype. The gene discussed is SHMT2; the disease is Parkinson disease.