RAB6A and Parkinson disease: The enhanced fission was found to be a result of interaction between LRRK2:G2019S and Drp‐1.160 The recruitment of Drp‐1 to mitochondrial and subsequent fission in PD patient‐derived fibroblasts and human SH‐SY5Y cells was found to be dependent upon LRRK2 kinase activity.161, 162 Given the recent identification of Rab GTPases, specifically Rab7,167 as bonafide LRRK2 substrates,168 it is likely that mutant LRRK2 activity could drive mitochondrial fragmentation observed in PD patients by assembling the protein machinery and activating membrane fusion.169