Foremost among these is whether there is a strong oxidant driver present, either oncogenic RAS (as we have shown) [26,27] or some other ROS-producing cancer-relevant mechanism, such as Akt hyperactivation or inflammation, leading to the chronically-elevated ROS levels required to produce sufficient levels of MTH1 substrates in the nucleotide pool, to evoke an integral role for MTH1. The gene discussed is NUDT1; the disease is cancer.