We then went on to demonstrate that elevated MTH1 levels facilitate transformation of immortalized cells via oncogenic RAS and enable maintenance of multiple tumor-promoting phenotypes, such as anoikis resistance and epithelial-mesenchymal transition (EMT), that rely on ROS-producing pathways, e.g., Akt or Rac1 signaling [26,32]. The gene discussed is NUDT1; the disease is neoplasm.