This also suggests that MutSα-mutated tumours display the unrepaired and potentially complete spontaneous deamination rate of 5-methylcytosine and that the MMR machinery plays a pivotal role in the repair at these sites, potentially guided by MBD4 for strand-discrimination in non-replicating dsDNA (Chen and Furano, 2015; Fang et al, 2021). The gene discussed is MBD4; the disease is neoplasm.