Functional studies showed that inhibition of PHD1-mediated Beclin1 P54 hydroxylation and autophagy by Beclin1 P54A knock-in expression or an autophagy inhibitor in combination with a HIF2α inhibitor treatment exhibited much-improved tumor growth inhibition compared to abrogation of autophagy or HIF2α alone. The gene discussed is EPAS1; the disease is neoplasm.