This variant has been observed in a single Taiwanese early-onset Parkinson disease patient and was absent from 508 ethnically matched controls (PMID:24339985).¹ Functional studies demonstrate that p.Arg767His robustly stimulates LRRK2 kinase activity >1.5-fold above wildtype by disrupting the ANK:C-terminal helix interface; this gain-of-function effect is consistent with the established pathogenic mechanism of LRRK2 in Parkinson disease (PMID:35950872).² The variant is present at very low frequency in gnomAD-Canada (AF=0.0163%, 3/18,414 alleles, 0 homozygotes), below the 0.1% PM2 threshold (gnomad_canada).³ Multiple in silico tools predict a benign effect: REVEL score 0.157, BayesDel score -0.0159304, and SpliceAI max delta 0.01, all consistent with no deleterious impact (revel, bayesdel, spliceai).⁴ This variant is classified as likely benign in ClinVar by a clinical diagnostic laboratory (VariationID 3571549, criteria provided, single submitter) (clinvar).⁵ Applying generic ACMG/AMP 2015 final classification combination rules (PMID:25741868): two supporting pathogenic criteria (PS3_supporting, PM2_supporting) and two supporting benign criteria (BP4_supporting, BP6_supporting) are present. These offset, resulting in a classification of Variant of Uncertain Significance.⁶