Base excision repair plays a significant role in protecting cells against oxidative DNA damage, single-strand breaks, and ROScancerogenesis. Any variation/mutation or expression dysregulation in BER could alter its function in favor of cancerogenesis. However, targeting such a repair system to induce massive oxidative DNA damage in cancer cells could be a potential therapeutic process forcing cancers to cell death.

Nevertheless, such an advanced targeted therapy seems challenging and needs further studies to avoid targeting normal cells and compensating their inhibition by activating other repair systems. Immunotherapy and BER inhibitors combination could be one of the solutions to target cancer cells specifically by targeting specific cancer cell receptors and inhibiting repair to induce cancer apoptosis. Such combinatorial therapy has already resulted in intriguing and exciting findings.