of uracil in DNA causing the fragmentation of newly synthesized DNA. Also, 5-FU is directly incorporated into DNA. UNG and SMUG1 are most likely to tackle the genomic incorporation of uracil and 5-FU during replication. Current research suggests that of SMUG1 but not UNG corresponds to increase in sensitivity to 5-FU. It was suggested that SMUG1 can be potentially used as a predictive biomarkers of drug response and a mechanism for acquired resistance in certain types of tumors. SMUG1 glycosylase is a key enzyme for repairing lesions generated during oxidative base damage. Investigation of SMUG1 expression in gastric cancers showed that overexpressed SMUG1 was correlated with patients’ poor survival. In gastric cancer inflammation is the driver for carcinogenesis. And thus one possible explanation is that cancer cells are under considerable oxidative stress compared to normal cells and unregulation of SMUG1 is essential for the repair of oxidative base damage and survival in cancer cells. In this case elevation of SMUG1 as opposed to depletion can be potentially used as a biomarker for survival. Interactions SMUG1 has been shown to interact with RBPMS and with DKC1. Interactive pathway map References Further reading