It has been shown in SH‐SY5Y cell cultures, neuronal cultures, conduritol‐β‐epoxide (CβE)‐treated mice, and transgenic Gba1 mouse models that reduced GCase activity results in increased α‐synuclein levels.7, 8, 9, 10, 11, 12, 13, 14 Conversely, it has been demonstrated in cell models that increased α‐synuclein causes a decrease in GCase activity.15 Moreover, the biochemical analysis of GBA1 wild‐type Parkinson patients showed that GCase activity and protein levels were significantly reduced in several brain regions,15, 16 further stressing the importance of GCase in PD development. The gene discussed is GBA1; the disease is Parkinsonism.