In fibroblasts derived from PD patients carrying LRRK2 G2019S, both the selective DRP1-inhibitor P110 or the expression of non-phosphorylatable mutant DRP1 T595A reverse the mitochondrial fragmentation and improve mitochondrial quality, indicating that LRRK2 G2019S-induced mitochondrial fragmentation is possible via a mechanism related to DRP1 T595 phosphorylation (Figure 2; Su and Qi, 2013). This evidence concerns the gene DNM1L and Parkinson disease.