While this topic is outside the scope of the present work, it seems important to underscore that all major human PD‐linked mutations (i.e., SNCA, LRRK2, PINK1, and DJ1) induce complex I inhibition, and synergism with the age‐dependent oxidative stress and inflammation further promotes increased generation of oxidative and nitrosative stress mediators, in turn exacerbating the proinflammatory microglial “M1” phenotype, then promoting progression of mDAn death (Lastres‐Becker et al., 2012). The gene discussed is LRRK2; the disease is Parkinson disease.