The mechanism can be concluded as follows: Targeting the ATP‐adenosine pathway via pharmacological blockade of CD39 and activation of AMPK not only promotes the accumulation of pro‐inflammatory eATP but also decreases the levels of immunosuppressive adenosine, thereby triggering an ATP‐dependent antitumor immunity by inducing pyroptosis in macrophages and improving DCs’ maturation, which allows for the activation of tumor‐specific CD8+ T and NK cells. Here, CD8A is linked to neoplasm.