Even during these early stages of the disease (pT1-2), there was over-expression of genes (LDHA, SLC2A1, HK2, SLC16A1, HK1) corresponding to proteins associated with glucose metabolism and solute transport functions that could potentially render the cancer cells more fit while at the same time imposing metabolic effects (nutrient deficiency and waste product toxicity) that restrict the TILs. This evidence concerns the gene SLC16A1 and cancer.