However, given the fact that increasing numbers of germline and somatic mutations within the exonuclease domain in human POLD1 and POLE have been identified in human cancers1,13,14 and that our in vitro nuclease assay, DNA elongation assay, and gap-filling assay clearly showed that MIF cooperates with Pol α and nuclease-deficient Pol δ to proofread DNA and ensure the success of DNA elongation, MIF is likely to play a role in proofreading in Pol δ- or Pol ε-deficient cancer cells. The gene discussed is POLE; the disease is cancer.