Both homozygous and heterozygous GBA1 mutations cause a reduction of glucocerebrosidase (GCase) activity and confer a 20‐ to 30‐fold increased risk for PD.1, 2, 3, 4 It is estimated that approximately 10 to 25% of PD patients have a GBA1 mutation (PD‐GBA1), with the most common mutations being L444P and N370S, and the highest frequency in Ashkenazi patients.1, 2, 3, 4. This evidence concerns the gene GBA1 and Parkinson disease.