Therefore, in these mouse models, the combination of the glutamine metabolism transporter inhibitor V‐9302 and anti‐PD‐1 therapy was more effective than was the monotherapy alone at promoting a sustained protective antitumor CD8+ T‐cell response and inhibiting the growth of implanted tumors in mice, further demonstrating that targeting the glutamine metabolism transporter SLC25A22 in tumor cells with V‐9302 can sensitize them to anti‐PD‐1 therapy through the dysregulation of immune‐related pathways. This evidence concerns the gene SLC25A22 and neoplasm.