Although further investigation is required to understand the detailed molecular mechanism of why there was specific reduction of NDUFS4 level in our mutant LRRK2 mice, our current findings are compatible with the specific reduction of mitochondrial Complex-I in human PD brains, and can help to explain why our mutant LRRK2 primary neurons were more susceptible to rotenone-induced ATP deficiency and cell death. This evidence concerns the gene LRRK2 and Parkinson disease.