The rate of the Miro1 defect was slightly lower in PD patients bearing mutations in LRRK2 or GBA in this cohort using iPSCs than that in the previous cohort using fibroblasts (iPSCs: 83.3 and 93.3%; fibroblasts: 100 and 100%, for LRRK2 and GBA, respectively). This evidence concerns the gene RHOT1 and Parkinson disease.