Stack et al. (2008) use a mouse model treated with MPTP, which selectively inhibits the activity of complex I thereby inducing a PD-like phenotype in a mouse model. The inhibition of complex I is associated with increased free radical production, less ATP output, and increases in apoptotic signals cytochrome c and caspase-3. Furthermore, the oxidative damage in the SN of PD patients contributes to mtDNA damage as has been seen in FRDA (Bhalla et al., 2016). The gene discussed is CASP3; the disease is Parkinson disease.