The above findings were extended to A549 human lung cancer cells in which doxycycline-inducible shRNA-mediated knockdown of endogenous Myc caused immediate proliferative arrest, a flattened morphology resembling that of Myc−/− fibroblasts, a two-fold reduction in mitochondrial mass, a ten-fold reduction in basal Oxphos and the complete failure to up-regulate Oxphos the usual two-three-fold in response to the Oxphos uncoupler FCCP and the glycolysis inhibitor 2-deoxyglucose [47]. The gene discussed is MYC; the disease is lung carcinoma.