To investigate the mechanistic basis of these observations—specifically how the N2081D variant affects LRRK2 function to increase CD risk and how its differences with the PD-associated G2019S variant might explain their distinct phenotypes—we generated a knock-in (KI) mouse model carrying the LRRK2 N2081D mutation using CRISPR/Cas9 gene editing. This evidence concerns the gene LRRK2 and Parkinson disease.