In the present study, blockage of the FD/LCS-activated mTOR/HIF1α signaling by the mTORC1 inhibitor, Rap, abrogated FD/LCS-promoted lungs’ glycolytic lactate production and exportation in lungs by significant inhibition of HK2 and MCT4 expressions to impede lactate supply for metastatic cancer use, and subsequently prevented LCS metastases development. The gene discussed is HIF1A; the disease is metastatic malignant neoplasm.