In addition to the inhibition of EGFR downstream PI3K/Akt and MAPK survival pathways, reductions in glucose uptake and glycolysis have been detected in gefitinib-treated lung cancer cells that precede cell cycle suppression and apoptosis induction [22], suggesting that glucose metabolic activity closely reflects the intrinsic response to EGFR TKI-based therapy. The gene discussed is AKT1; the disease is lung carcinoma.