Aerobic glycolysis is increased in prostate cancer due in part to genomic loss of the PTEN (phosphatase and tensin homolog) locus, leading to activation of the PI3K/AKT pathway, and 8q amplification, including of the Myc gene, which occurs in up to 70% and 30% of prostate cancers, respectively [7]. The gene discussed is AKT1; the disease is prostate carcinoma.