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 MUTYH and cancer.