In our study, treatment of LKB1−/−NIC mice that are hyperactive for mTOR and metabolically active (Fig. 6A) with 2-DG mono-therapy (Fig. 3 and 6B) inhibited tumorigenesis, such that both tumor volume and burden were reduced in response to reduced aerobic glycolysis and mitochondria function, however AZD8055 mono-therapy (Fig. 3 and 6C) was significantly better at inhibiting tumor volume, burden and mitochondrial function. This evidence concerns the gene STK11 and neoplasm.