KRAS and cancer: Abnormal activation of Kirsten rat sarcoma viral oncogene homolog (KRAS) and the amplification of MYC protooncogene (MYC) in cancer enhance the catabolism of glutamine as the carbon source of the tricarboxylic acid cycle, increasing the ROS generation by ETC [76, 77]; mutant KRAS can also increasing mitochondrial ROS via decreasing the stabilization of electron transport and leading to the leakage of electrons [78]; B-cell lymphoma 2 (Bcl-2) is overexpressed in a variety of tumors which can affect the activity of ETC by interacting with cytochrome C oxidase [79].