Recent studies also highlight that NSCLC cells activate the purine–PD-L1 axis through CXCL8-mediated macrophage recruitment, and glutamine antagonist DRP-104 can enhance ICI efficacy by inhibiting purine biosynthesis [19], providing experimental evidence for the metabolic-immune regulatory mechanisms discussed. The gene discussed is CXCL8; the disease is non-small cell lung carcinoma.