The documented protection of normal tissues from drug-induced toxicity by selenium may be due in part to the activation of Nrf2, resulting in diminished levels of reactive oxygen species, activation of PHDs, which are enzymes that regulates the degradation of HIFs in response to oxygen availability (resulting in enhanced HIF hydroxylation and degradation), and activation of the DNA-repair genes (resulting in enhanced DNA repair involved in tumor cell chemo- and radio-resistance via the Nrf2/Kelch-like ECH-associated protein 1 (Nrf2/Keap1) pathway) [51,52]. The gene discussed is KEAP1; the disease is neoplasm.