The results of this study suggest that alteration of the metabolic phenotype of PTC by mitochondria-targeting agents, particularly in terms of ATP production efficiency, can influence tumor suppression; the effects include the inhibition of tumor proliferation, migration, and invasion, along with obstruction of the cell cycle and acceleration of apoptosis via the PI3K/Akt/FoxO1/Cyclin D1 pathway. The gene discussed is CCND1; the disease is neoplasm.