Consistently, the treatment of 6-OHDA with Csn-B downregulated the PI3K/AKT viability pathway, indicating that serious ER stress was activated to produce obvious apoptosis in the in vitro PD model (p-AKT: 50.4% of the control group in 6-OHDA group, 38.6% in the Csn-B + 6-OHDA group, n = 5 independent experiments, ***p < 0.001; p-PI3K: 52.4% of the control group in 6-OHDA-treated group, 38.6% in the Csn-B + 6-OHDA group, n = 5 independent experiments,***p < 0.001, Fig. 3F). The gene discussed is AKT1; the disease is Parkinson disease.