Given that epigenetic changes affecting gene expression and overexpression of histone deacetylases (HDACs) in cancer commonly cause resistance to genotoxic-based therapies, our dual-target approach, combining an ATM activator with an HDAC inhibitor, may harness the benefits of ATM activation while enhancing chemotherapy effectiveness and minimizing resistance, potentially improving treatment outcomes. This evidence concerns the gene HDAC9 and cancer.