Prospective patient selection may also enhance NDV outcomes: (i) Type-I IFN pathway attenuation (e.g., IFNAR/STAT alterations) predicts permissive replication [98]; (ii) tumor hypersialylation supports NDV binding [22]; (iii) TME state (baseline chemokines, M1/M2 ratio) and metabolic features (acidosis/hypoxia signatures) may indicate likelihood of NDV-mediated “hot-switching” [99, 100]; and (iv) CAR-T cell target stability plus PD-L1 dynamics inform the need for NDV-encoded checkpoint blockade [101]. The gene discussed is CD274; the disease is neoplasm.