As Tax can damage tumor cell mitochondria and lead to ROS production, and inhibiting autophagy can lead to the inability to clear damaged mitochondria, resulting in excessive ROS accumulation, which will in turn activate the death-related pathways, leading to increased cell death [48], we had reason to speculate that α-Hed exerted its synergistic effect on Tax through such a pathway, and Figure 6 proves us correct. The gene discussed is CNTN2; the disease is neoplasm.