In 2014, Shimura et al. reported how radioresistance is influenced by serine/threonine kinase (AKT)-mediated enhanced aerobic glycolysis acquired by tumor cells [54], demonstrating that radioresistant cells have higher lactate production rates and enhanced aerobic glycolysis compared with parental cells, thus suggesting that tumor cell metabolic pathway, in which mitochondria play a key role, is an attractive target to eliminate radioresistant clones and improve RT efficacy. This evidence concerns the gene AKT1 and neoplasm.