Genetic loss of TNF and its death-signaling molecules (e.g., Tnfr1 and Casp8) led to uncontrolled tumor growth, whereas loss of molecules involved in ubiquitinating RIPK1 (e.g., Traf2 and Birc2/3) resulted in tumor rejection following immune checkpoint blockade (69, 73–75). The gene discussed is TRAF2; the disease is neoplasm.