Since both CI and CII mediate electron transfer to CIII31 and because mitochondrial metabolism and consequent ROS generation are crucial for KRAS-induced tumorigenesis56, it is possible that cancer cells carrying mutant KRAS may acquire alternative strategies such as upregulation of CII to maintain essential mitochondria functions; furthermore, relatively increased dependence on CII activity may be a mechanism underlying the increased sensitivity to gracillin treatment in KRAS mutant cancer cells. This evidence concerns the gene KRAS and cancer.