LRRK2 has been shown to colocalize to mitochondria and interact with a number of key regulators of mitochondrial fission/fusion (Stafa et al., 2014; Wang et al., 2012), thus raising the possibility that LRRK2 may lead to PD pathogenesis by disrupting mitochondria function when overexpressed or mutated (Biskup et al., 2006). Here, LRRK2 is linked to Parkinson disease.