Furthermore, the presence of CXCR6, together with IL-15 trans-presentation within the tumor milieu, is critical for sustaining effector-like CTL survival and local proliferation, thereby boosting their antitumor capacity—particularly before terminal exhaustion sets.45 In hepatic tissue, CXCL16 produced by sinusoidal endothelial cells attracts and stimulates CXCR6+ NKT cells, augmenting antitumor responses through elevated cytokine release such as IFN-γ.46–49 In the present study, we detected robust signaling between tumor-derived CXCL16 and CXCR6 on HLA-DR+CD38+CD8+ T cells. The gene discussed is CXCR6; the disease is neoplasm.