Our results showed that ZSD treatment significantly decreased the expression level of p-AKT, p-GSK-3β, and β-catenin and increased that of ROS-induced mitochondria-dependent apoptosis Bax/Bcl-2 and cleaved caspase-3 in lung cancer cells both in vivo and in vitro, indicating that ZSD treatment may induce cancer cell apoptosis via the AKT/GSK-3β/β-catenin pathway. Here, GSK3B is linked to peroxisome biogenesis disorder.