In contrast, several reports have shown that a high level of ROS, which is generated either during respiration or in a targeted manner by a class of NADPH oxidases, maintains protumorigenic signaling, resulting in a loss of tumor suppressor gene function, adaptations to hypoxia, increased glucose metabolism, and resistance to apoptosis attribute to strives to scavenge excessive ROS [21]. This evidence concerns the gene FMO5 and neoplasm.