BV increased cell viability, decreased amyloid β-protein (Aβ) accumulation in U87MG AD mimic cells, as well as suppressed inflammatory reaction through inhibiting the mRNA expression of IL-1, TNF-α and cyclooxygenase-2 (COX-2), and prevented apoptosis by reducing the expression level of Caspase-3, indicating that BV could be a potential AD therapeutic drug (Ku et al., 2020). The gene discussed is CASP3; the disease is Alzheimer disease.