UNG and neoplasm: Hence, the two enzymes complement each other during the repair of uracil in vivo and the mutagenic potential of defective uracil repair is best assessed in cells lacking both enzymes: whole genome sequencing of UNG/SMUG1-deficient tumours revealed that the loss of uracil repair by UNG and SMUG1 primarily leads to C to T transition mutagenesis at CpG dinucleotides.