,110 Acute degradation dysregulates TNFR1/TLR3/4 signalling, potentiating NF-κB/MAPK/IFN outputs and sensitising tumours to TNF/IFN, thereby reversing the cold tumour phenotype; concurrently, disruption of the TRADD-RIPK1 complex drives TRADD-dependent RIPK3 activation, promoting apoptosis while inhibiting pro-survival pathways (e.g., NF-κB pathways).69 The gene discussed is TNFRSF1A; the disease is neoplasm.