In order to investigate the interplay between hMTH1- and hMYH-dependent BER, we utilized MMR defective T-cell acute lymphoblastic leukemia (T-ALL) cells.17 Malfunctioned MMR and the consequent microsatellite instability are highly frequent in T-ALL and thus simplify our study model.18, 19, 20, 21 In addition, RNA-sequencing analysis of over 900 human cancer cell lines revealed that T-ALL cells have the highest expression for both MTH1 and MYH, making them an ideal model for this study22 (Supplementary Figure S2). This evidence concerns the gene MRC1 and acute lymphoblastic leukemia.