Moreover, Rev1 functions together with Polζ in TLS that occurs during gap filling reactions in human or mouse cells (Yoon et al, 2015) and the dependence of cancer cells upon Rev1/Polζ for DNA damage induced mutagenesis (Doles et al, 2010; Xie et al, 2010) suggests that during malignant transformation, cancer cells acquire the potential of highly elevated mutability, afforded by Rev1/Polζ. Here, REV3L is linked to cancer.