Activation of AMPK enhances expression of PGC1-α and its target genes in cancer cells under glucose-limiting conditions.3 Moreover, inhibition of mTOR by rapamycin increases the expression of PGC1-α,10 suggesting that mTOR inversely correlates with PGC1-α expression, and it might be a negative regulator of mitochondrial biogenesis.3 Activation of AMPK with concomitant inhibition of mTOR is decisive in maintaining energy homeostasis and mitochondrial function (Figure 1). The gene discussed is MTOR; the disease is cancer.