As an environment factor, rotenone selectively inhibits mitochondrial complex I, causing mitochondrial impairment via oxidative stress, and resulting in an increase of apoptotic markers of neurons such as caspase-3 activity, caspase-9 activity, Bax expression, cytochrome c, lactate dehydrogenase release and microtubule destabilization in rotenone-evoked Parkinsonism [29–34]. This evidence concerns the gene CASP3 and Parkinsonism.