It has been suggested that processing of mis-incorporated 8-oxodG opposite dA is mainly mediated by post-replicative MMR in mammalian cells.13 In addition, hMYH activity has been shown to be required for removal of dA from the nascent strand when mispaired with 8-oxodG,14 and there is also cumulative evidence suggesting hMYH has physical interactions as well as functional cooperation with MMR.14, 24 Using data base mining, we observed MYH and MTH1 expression levels are particularly high in T-ALL (Supplementary Figure S2). The gene discussed is MRC1; the disease is acute lymphoblastic leukemia.