The identification of several genes causing monogenic forms of PD (e.g. α-synuclein [SNCA], Parkin, DJ-1, PINK1, LRRK2) has led to the generalized view that protein misfolding, mitochondrial dysfunction, impaired oxidative stress response, and altered function of the ubiquitin-proteasome system are central pathogenic mechanisms underlying the familial forms of PD [1]. This evidence concerns the gene LRRK2 and Parkinson disease.