Notably, non-manifesting genetic carriers bearing mutations in LRRK2 or GBA showed a similar rate of the Miro1 defect as symptomatic patients carrying mutations in the same gene (carriers: 86.4 and 83.3%; PD: 83.3 and 93.3%, for LRRK2 and GBA, respectively). This evidence concerns the gene LRRK2 and Parkinson disease.