In non-small cell lung cancer cells, the genetic disruption of the MCT’s chaperone CD174 was described to lower the glycolytic rate 2.0- to 3.5-fold, and to stimulate mitochondrial respiration, thereby making CD174-null cells particularly sensitive to inhibitors of mitochondrial respiration both in vitro and in vivo [87,88]. The gene discussed is FUT3; the disease is non-small cell lung carcinoma.