Thus, high levels of ROS present in tumor cells could result from either an amplified metabolic activity, mitochondrial dysfunction, peroxisome activity, deregulated cell receptor signaling, oncogene activity, enhanced activity of cyclooxygenase, lysyl oxidase, and thymidine phosphorylase, or communication with the immune infiltrate (Babior, 1999; Storz, 2005), suggesting that ROS and RNS can support numerous facets of tumor development and progression. Here, TYMP is linked to neoplasm.