Of note, AMPK activation is thought not only to straightforwardly reduce tumor burden by inhibiting cancer cell growth but also to concurrently support the expansion and survival of tumor-infiltrating lymphocytes (TILs), especially CD8+ T cells within the TME, in part by the inhibition of glycolysis and promotion of oxidative phosphorylation [81,82,83,84]. This evidence concerns the gene PRKAA1 and neoplasm.