In the last few decades, numerous studies have demonstrated that adenosine signaling involving CD39/CD73 ectonucleotidases expressed on tumor cells is a critical pathway in TME to evade the immune surveillance and generate an immunosuppressive milieu.[42, 43, 44] Although the immunosuppressive role of adenosine has been established in various malignancies, including NSCLC, this study provides critical insights into how adenosine production in EGFR‐mutant TME disrupts DC functionality, representing a significant advance in understanding its impact on anti‐tumor immunity. The gene discussed is ENTPD1; the disease is neoplasm.