Considering the data showing efficacy of GT-02216 also in wild-type cells, our study prompts additional investigations to further underpin that, despite the fact that GBA1 mutations are not linked to Alzheimer’s disease or other neurodegenerative proteinopathies besides Parkinson’s disease57,58, boosting GCase activity could represent a viable therapeutic strategy to slow-down aging-dependent protein deposition in the general patient population not affected by GBA1 mutations. The gene discussed is GBA1; the disease is early-onset autosomal dominant Alzheimer disease.