Figure 3 shows that APS suppress the Wnt/β-catenin signalling pathway by downregulating the key oncogenic targets, including β-catenin, C-myc, and cyclin D1, which subsequently reduces Bcl-2 expression and activates the apoptotic cascade in HepG2 liver cancer cells. Concurrently, APS induce ferroptosis by altering redox homeostasis—marked by reduced glutathione (GSH), increased ROS, elevated lipid peroxidation, and intracellular Fe2+ accumulation. The gene discussed is BCL2; the disease is liver cancer.