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Diagram showing the induction of DNA damage by radiation or doxorubicin, and the effect of KMT inhibitors on DDR. Both inhibitors promote the generation of DNA damage, impair its repair and thus contribute to facilitate tumor cell death. The SUV39H1, EZH2, SETD8, and NSD2, which mediate H4 lysine methylation, would be the most probable candidate enzymes inhibited by chaetocin and/or tazemetostat and explain why H4K20me2 levels decrease in presence of both KMT inhibitors.
