GBA1 and Parkinson disease: 2009; Bultron et al. 2010; McNeill et al. 2012a). This compares with leucine‐rich repeat kinase 2 mutations that are estimated to cause 0.5% of sporadic PD. Further, even in patients without GBA1 mutations, a decrease in GCase activity is still found in all studied cases, suggesting that this protein plays a much more important role in PD than previously appreciated. As such, further studies of GBA1, in particular of treatments that increase levels of GCase, are likely to be one of the most promising future avenues for tackling PD.