Liver cancer is affected by adenosine expression and metabolic byproducts. Cancer patients treated with different adenosine antagonists had their pathological alterations rectified by influencing proliferation, apoptosis, and angiogenesis. Our review focuses on new carcinogenic mechanisms driving adenosine activity, especially changes in immunological mediators and immune archetypes. In this study, we look at how adenosine affects the reprogramming of tumor immune cells like dendritic cells, T cells, Tregs, and neutrophils. This study covers current knowledge of the molecular mechanisms underlying adenosine's unique carcinogenic mechanisms via modification of the expression pattern of immune mediators in the tumor immune microenvironment, such as PD-1, CTLA-4, TGF-β, and IL-12, IL-23, and FOXP3. Adenosine reprograms tumor immunological architecture and mediators, making it a viable therapeutic target for tumor eradication through its multiple mechanisms of carcinogenicity.