More clinically significant, we demonstrate that the FD/LCS-driven lactate metabolic vulnerability for LC metastases can be therapeutically targeted by Met, the conventional anti-diabetic medicine, which has been under extensive pre-clinical investigation and clinical trials for its therapeutic effect of lung cancers [48,49] Resembling the Rap effect, Met treatment inhibited FD/LCS-activated mTORC1 signaling by suppressed expression of mTORC1/HIF-1α signalers, and decreased HKII and the MCT4 lactate exporter to result in Met normalizing lungs’ lactate levels. This evidence concerns the gene HIF1A and lung carcinoma.