The supplementation of doxorubicin-resistant colon cancer and malignant pleural mesothelioma cells, constitutively expressing HIF-1α, with pyruvate restores the sensitivity to doxorubicin: the mechanisms is similar to that of DCA, because pyruvate increases ETC and suppresses glycolysis [216], reversing the metabolic phenotype supported by HIF-1α. This evidence concerns the gene HIF1A and malignant pleural mesothelioma.