Rev1, a member of the Y family polymerases, plays a key role in the translesion synthesis (TLS) pathway. TLS is an error-prone process that enables cells to overcome replication blockage caused by DNA damage, safeguarding genome integrity and cell survival [1,4].

Rev1-mutated mouse models, such as the Rev1 transgenic (Tg) mouse, have been used to study its role in mutagenesis and carcinogenesis. In Rev1-Tg mice treated with N-methyl-N-nitrosourea (MNU), the mutation frequency in thymic lymphoma (TL) was higher compared to wild-type (WT) mice, and pre-leukemic cells were detected earlier in Rev1-Tg mice. This indicates that Rev1 overexpression accelerates mutagenesis and MNU-induced TL [3]. In lung cancer, REV1 silencing decreased the growth and proliferation of lung cancer cells, and a novel inhibitor JH-RE-06 suppressed lung tumorigenesis, suggesting REV1 as a potential diagnostic marker and therapeutic target [2].

In conclusion, Rev1 is crucial in the TLS pathway, influencing mutagenesis and carcinogenesis. Mouse models, especially Rev1-Tg, have provided insights into its role in thymic lymphoma and lung cancer, highlighting its significance in understanding tumorigenesis mechanisms and potentially developing cancer therapies.