In line with the malignant phenotype of lactate-metabolizing signatures, our data demonstrated that the FD/LCS-metastatic mice reprogrammed lung/metastatic tumors’ fuel metabolism from mt OXPHOS, by suppressed expression of PDH and mt VDAC, to accelerated aerobic glycolysis, by increased expression of HK2, LDHA, and PKM2, for lactate over-production. This evidence concerns the gene PKM and metastatic neoplasm.