LRRK2 and Parkinson disease: While previous studies have proved that R1441C/G/H mutations can both increase binding affinity for GTP and decreas GTPase activity to varying degrees, our present study expounded from the previously-unnoted aspect that such mutations were also likely to speed up the conformational transition during the GTPase activation cycle to trap ROCs in a more persistently active state, which would ultimately contribute to LRRK2 dysfunction and PD pathogenesis.