As further proof of concept for this strategy, silencing or inhibition of the mitochondrial protease ClpP, which normally degrades mitochondrial proteins damaged by oxidative stress, was shown to be an effective anti-tumor strategy, and a ClpP inhibitor was shown to delay tumor growth in an animal model of acute myeloid leukemia [19, 20]. The gene discussed is CLPP; the disease is acute myeloid leukemia.