Inflammation and chronic infections play critical roles in promoting and exacerbating cancer. Chronic inflammation creates a tumor-supporting microenvironment, and cytokines produced by activated innate immune cells stimulate tumor growth and progression. Inflammatory cells also produce cytokines that can limit tumor growth. The review discusses the mechanisms linking inflammation, innate immunity, and cancer, focusing on cytokines such as TNF-α, TRAIL, IL-6, IL-17, IL-12, IL-23, IL-10, and TGF-β. These cytokines can either promote or inhibit tumor development, depending on their context and the tumor microenvironment. TNF-α promotes tumor growth by inducing antiapoptotic molecules and enhancing angiogenesis and metastasis. TRAIL, on the other hand, induces apoptosis in tumor cells but can be ineffective if NF-κB is active. IL-6 is a key growth-promoting and antiapoptotic factor that supports tumor development. IL-17 enhances inflammation and tumor progression by promoting angiogenesis and recruiting immune cells. IL-12 and IL-23 promote Th1 and Th17 responses, which can enhance tumor growth or suppress it depending on the context. IL-10 and TGF-β have dual roles, with IL-10 generally inhibiting tumor growth and TGF-β acting as a tumor suppressor in early stages but promoting progression in later stages. The review highlights the complex interplay between cytokines and the tumor microenvironment, emphasizing the importance of targeting proinflammatory cytokines and enhancing the activity of anti-inflammatory and proapoptotic cytokines for cancer therapy. Understanding these mechanisms provides opportunities for developing targeted therapies that modulate cytokine signaling and NF-κB activation to combat cancer.Inflammation and chronic infections play critical roles in promoting and exacerbating cancer. Chronic inflammation creates a tumor-supporting microenvironment, and cytokines produced by activated innate immune cells stimulate tumor growth and progression. Inflammatory cells also produce cytokines that can limit tumor growth. The review discusses the mechanisms linking inflammation, innate immunity, and cancer, focusing on cytokines such as TNF-α, TRAIL, IL-6, IL-17, IL-12, IL-23, IL-10, and TGF-β. These cytokines can either promote or inhibit tumor development, depending on their context and the tumor microenvironment. TNF-α promotes tumor growth by inducing antiapoptotic molecules and enhancing angiogenesis and metastasis. TRAIL, on the other hand, induces apoptosis in tumor cells but can be ineffective if NF-κB is active. IL-6 is a key growth-promoting and antiapoptotic factor that supports tumor development. IL-17 enhances inflammation and tumor progression by promoting angiogenesis and recruiting immune cells. IL-12 and IL-23 promote Th1 and Th17 responses, which can enhance tumor growth or suppress it depending on the context. IL-10 and TGF-β have dual roles, with IL-10 generally inhibiting tumor growth and TGF-β acting as a tumor suppressor in early stages but promoting progression in later stages. The review highlights the complex interplay between cytokines and the tumor microenvironment, emphasizing the importance of targeting proinflammatory cytokines and enhancing the activity of anti-inflammatory and proapoptotic cytokines for cancer therapy. Understanding these mechanisms provides opportunities for developing targeted therapies that modulate cytokine signaling and NF-κB activation to combat cancer.