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Monogenic forms of Parkinson's disease (PD) have demonstrated a heterogeneous disorder involving multiple biological pathways.1 Familial forms of PD have been linked to variants in LRRK2, SNCA, VPS35, PARKIN, and PINK1.1 Heterozygous GBA mutation carriers are associated with higher disease risk, earlier onset, and accelerated clinical progression.1 Recently, RAB32 has emerged as a nominated PD gene. It encodes a Rab GTPase involved in mitochondrial and vesicular trafficking pathways. A rare substitution, p.Ser71Arg (rs200251693), has been proposed as a potential susceptibility factor.2, 3 Reported carriers exhibit late-onset, levodopa-responsive parkinsonism with familial clustering; the only available autopsy case lacked Lewy bodies.1-3 Across published studies, RAB32 c.213C>G was detected in 0.22% to 2.3% of patients, primarily within Mediterranean and North American cohorts, and was absent in large East Asian datasets. This pattern suggests regional specificity and a possible shared Mediterranean haplotype.2-6 Limited data exist from several regions, including Eastern Europe, Ireland, sub-Saharan Africa, and South America. To address this gap, we screened 1730 patients with PD from Colombia (n = 188), Czech Republic (n = 31), Ecuador (n = 390), Ireland (n = 314), Nigeria (n = 52), Poland (n = 627), and Ukraine (n = 128). We analyzed 523 healthy control subjects from Colombia, Ireland, Poland, and Ukraine. Genotyping was performed at Mayo Clinic Florida. No carriers were identified (Table 1, Supporting Information Table S1, Fig. 1). Age at onset was typically in the late 50s to early 60s in the Czech, Ecuadorian, Nigerian, Polish, and Ukrainian groups, whereas the Colombian cohort demonstrated a younger disease onset. Family history was highest in Ireland (57%) and Ukraine (45%). Interestingly, Ireland exhibits one of the highest GBA carrier rates in Europe and a low LRRK2 mutation frequency.7 Absence of RAB32 p.Ser71Arg suggests that vesicular-trafficking pathways may play a lesser role in Irish PD relative to lysosomal pathways.7 Although case–control imbalance limits formal association testing, and may reduce statistical power, the complete absence of the allele suggests extremely low frequency across these populations. Several factors may explain this observation: first, only a single variant (albeit the only one implicated in PD to date) was tested rather than performing full gene or exome sequencing, which is a major limitation. This is similar to VPS35 p.D620N, another single rare variant whose overall contribution to clinical PD risk is minimal due to the very low frequency.1, 7 Second, sampling strategies differed across countries, including early-onset enrichment in Colombia and clinic-based recruitment in Nigeria. Finally, evaluating extremely rare variants requires sample sizes in tens of thousands. Our findings should be interpreted as exploratory rather than definitive regarding the variant's global contribution to PD. This work emphasizes the importance of increasing diversity in PD genetics research. Underrepresentation of African and South American populations persists, although initiatives such as the Global Parkinson's Genetics Program (GP2) and The Latin American Research consortium on the GEnetics of Parkinson's disease (LARGE-PD) are actively addressing these gaps and have already produced important contributions from both regions. In conclusion, among 1730 patients with PD from selected African, European, and South American cohorts, no RAB32 p.Ser71Arg carriers were identified. Broader, sequence-based, globally inclusive studies will be essential to clarify the role of nominated rare variants like RAB32 in PD pathobiology and therapeutic development. 1. Research project: A. Conception, B. Organization, C. Execution; 2. Statistical Analysis: A. Design, B. Execution, C. Review and Critique; 3. Manuscript: A. Writing of the first draft, B. Review and Critique. D.A.O.: 2A, 2B, 2C, 3A, 3B. A.I.S.-B.: 2A, 2B, 3B. A.M.: 2B, 3B. C.C.-C.: 2B, 3B. I.R.: 2B, 3B. F.A.: 2B, 3B. G.J.-K.: 2B, 3B. J.S.: 2B, 3B. M.R.-B.: 2B, 3B. A.P.: 2B, 3B. K.K.: 2B, 3B. S.O.: 2B, 3B. O.A.R.: 2A, 2B, 2C, 3B. T.L.: 2A, 2B, 2C, 3B. Z.K.W.: 2B, 3B. D.A.O. receives research support from The Michael J. Fox Foundation. A.I.S.-B., A.M., C.C.-C., I.R., F.A., G.J.-K., J.S., M.R.-B., A.P., K.K., S.O., O.A.R., and T.L. declare no financial disclosures. Z.K.W. is partially supported by the National Institutes of Health (NIH)/National Institute on Aging and NIH/ National Institute of Neurological Disorders and Stroke (1U19AG063911), the Haworth Family Professorship in Neurodegenerative Diseases fund, Albertson Parkinson's Research Foundation, PPND Family Foundation, and Margaret N. and John Wilchek Family; he serves as principal investigator (PI) or co-PI on Biohaven Pharmaceuticals, Inc. (BHV4157-206), ONO-2808-03, and Amylyx AMX0035-009 projects/grants; he serves as co-PI of the Mayo Clinic APDA Center for Advanced Research, as an external advisory board member for the Savanna Biotherapeutics, Inc., and as a consultant for Eli Lilly & Company. Author disclosures are available in the Supporting Information. The data that support the findings of this study are available from the corresponding author upon reasonable request. Table S1. Detailed phenotypic characterization of the Irish cohort of patients with Parkinson's disease divided by the age-at-onset. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.