NAF1 and cancer: These studies reveal that cancer cells accumulate high levels of NAF-1, and that disrupting NAF-1 function, for example by a point mutation in the NAF-1 [2Fe-2S] cluster-binding domain, or by suppressing NAF-1 protein expression using shRNA, results in enhanced levels of mitochondrial labile iron and ROS levels that trigger apoptosis of cancer cells [14,16,18,22,24].