In our LKB1−/−NIC mouse model of primary breast cancer, LKB1-AMPK signaling is significantly compromised, thus mono-therapy with the dual ATP-competitive PI3K/mTOR inhibitor NVP-BEZ235 was insufficient to block tumorigenesis whereas the combination of NVP-BEZ235 and AZD8055 resulted in reduced mitochondria function comparable to AZD8055 mono-therapy alone. This evidence concerns the gene STK11 and breast carcinoma.