Reactive oxygen species (ROS) are crucial in modulating physiological functions and are involved in both inflammation and cancer. This review explores the roles of ROS in normal cells, inflammation, and cancer, highlighting their impact on immune responses and cancer therapy. ROS are generated through various pathways, including mitochondrial respiration, NADPH oxidases, and enzymatic reactions. They play a dual role in cancer, promoting tumorigenesis while also inducing apoptosis in cancer cells. ROS are essential for immune cell function, influencing signaling pathways such as NF-κB, JNK, and MAPK, which regulate cell survival, death, and proliferation. ROS also contribute to the regulation of transcription factors like NRF2 and HIF-1α, which are critical for maintaining redox homeostasis and tumor progression. In the tumor microenvironment (TME), ROS can promote cancer cell survival and immune evasion by modulating the activity of immune cells such as T cells, myeloid-derived suppressor cells (MDSCs), and macrophages. ROS can also enhance the immunosuppressive environment by inducing apoptosis of regulatory T cells and promoting the differentiation of immunosuppressive macrophages. The review emphasizes the potential of targeting ROS and its modulators as novel therapeutic strategies in cancer immunotherapy. It also discusses the role of ROS in cancer immunity, including its impact on existing immunotherapies such as immune checkpoint blockade, chimeric antigen receptors, and cancer vaccines. The study highlights the importance of understanding ROS-mediated mechanisms to develop more effective cancer treatments and personalized therapies.Reactive oxygen species (ROS) are crucial in modulating physiological functions and are involved in both inflammation and cancer. This review explores the roles of ROS in normal cells, inflammation, and cancer, highlighting their impact on immune responses and cancer therapy. ROS are generated through various pathways, including mitochondrial respiration, NADPH oxidases, and enzymatic reactions. They play a dual role in cancer, promoting tumorigenesis while also inducing apoptosis in cancer cells. ROS are essential for immune cell function, influencing signaling pathways such as NF-κB, JNK, and MAPK, which regulate cell survival, death, and proliferation. ROS also contribute to the regulation of transcription factors like NRF2 and HIF-1α, which are critical for maintaining redox homeostasis and tumor progression. In the tumor microenvironment (TME), ROS can promote cancer cell survival and immune evasion by modulating the activity of immune cells such as T cells, myeloid-derived suppressor cells (MDSCs), and macrophages. ROS can also enhance the immunosuppressive environment by inducing apoptosis of regulatory T cells and promoting the differentiation of immunosuppressive macrophages. The review emphasizes the potential of targeting ROS and its modulators as novel therapeutic strategies in cancer immunotherapy. It also discusses the role of ROS in cancer immunity, including its impact on existing immunotherapies such as immune checkpoint blockade, chimeric antigen receptors, and cancer vaccines. The study highlights the importance of understanding ROS-mediated mechanisms to develop more effective cancer treatments and personalized therapies.