This study clarifies the interaction between autophagy and inflammasome within the cancer framework. The inflammasome generates pro-inflammatory cytokines to direct the immune response to pathogens and cellular stressors. Autophagy maintains cellular homeostasis and can either promote or inhibit cancer. These pathways interact to affect tumorigenesis, immune responses, and therapy. Autophagy controls inflammasome activity by affecting cancer pathogenesis and tumor microenvironment inflammation, highlighting novel cancer therapeutic approaches. Recent studies indicate that modulating autophagy and inflammasome pathways can boost anti-cancer immunity, reduce drug-resistance, and improve therapeutic efficacy. Recent studies indicate modulating inflammasome and autophagy pathways can augment anti-cancer immunity, mitigate therapy resistance, and improve treatment efficacy. Cancer research relies on understanding the inflammasome-autophagy relationship to develop targeted therapies that enhance anti-tumor efficacy and reduce inflammatory symptoms. Customized therapies may improve outcomes based on autophagy gene variations and inflammasome polymorphisms. This study investigates autophagy pathways and the inflammasome in tumor immunopathogenesis, cytokine function, and cancer therapeutic strategies, highlighting their significance in cancer biology and treatment.