Less than 1 year after the discovery of mutations in LRRK2, it was possible to clone LRRK2, develop reasonable polyclonal antibodies (Abs), and create an initial assay to measure LRRK2 kinase activity.25 During this time, some reports, based on homologous modifications made to other protein kinases, suggested that PD mutations would inhibit kinase function.26 In contrast, the first actual assay demonstrated an activating effect for the R1441C and G2019S with respect to LRRK2 autophosphorylation.25 This evidence concerns the gene LRRK2 and Parkinson disease.