Gamma delta (γδ) T cells represent a minor yet functionally important lymphocyte population with considerable potential in cancer immunotherapy. Owing to their MHC-independent cytotoxic activity, γδ T cells can recognize and eliminate a broad range of tumor cells, making them attractive candidates for adoptive cell therapy. In addition, the infiltration of γδ T cells within tumor tissues has been associated with improved clinical outcomes, further supporting their therapeutic relevance. Dasatinib, an FDA-approved tyrosine kinase inhibitor with reported immunomodulatory and senolytic properties, has recently gained attention for its ability to regulate immune cell function. In CAR-T cells, dasatinib has been shown to induce a reversible resting-like state, thereby controlling differentiation, limiting exhaustion, and improving anti-tumor activity. However, the effects of dasatinib on γδ T cells, particularly during ex vivo expansion, remain poorly understood. In this study, we investigated the impact of dasatinib treatment during γδ T cell expansion. Dasatinib exposure promoted a resting-like phenotype in γδ T cells and significantly improved cell viability and proliferation compared with conventional culture conditions, suggesting its potential utility in optimizing cell therapy manufacturing. Moreover, dasatinib-treated γδ T cells exhibited enhanced cytotoxicity against selected cancer cell lines and showed altered expression of immune checkpoint molecules. These findings indicate that dasatinib-mediated modulation of γδ T cells may contribute to the development of more effective γδ T cell-based cancer immunotherapies and support their application as off-the-shelf allogeneic cell therapy products.