Such reduced GCase activity may play a role as disease modifier, and it will be important to assess GCase activity from a larger set of LRRK2 PD patient-derived cells, and determine whether the decrease in GCase activity correlates with a detectable increase in the lipids which serve as substrates for the enzyme, which may then be able to trigger α-synuclein accumulation. Here, LRRK2 is linked to Parkinson disease.