Recently, we have not only identified PD patients carrying heterozygous mutations on MIRO17,8, but we also demonstrated that the MIRO1 p.R272Q mutation, affecting the 1st EF-hand Ca2+-binding domain, is sufficient to promote loss of tyrosine hydroxylase (TH)-positive dopaminergic neurons in aged knock-in mice and patient-specific iPSC-derived midbrain organoids9. Here, RHOT1 is linked to Parkinson disease.