On the immune axis, IR has a dual face: cGAS–STING–dependent type I interferon can promote antitumor priming, yet PD‐L1 is frequently upregulated on tumor and myeloid populations post‐RT, reinforcing local immunosuppression and selection for exhaustion phenotypes; these dynamics motivate combinations with checkpoint blockade and chemokine‐axis modulators (e.g., CXCL12/CXCR4 inhibitors) to counteract maladaptive remodeling [115]. The gene discussed is CGAS; the disease is neoplasm.