Caspase 8 enzymatic activity negatively regulates necroptosis via RIPK1 and RIPK3 instability [42], and we found that type I IFNs limited caspase expression during infection, providing a potential mechanism whereby IFNα/β facilitate pathologic RIPK1-RIPK3 interaction and downstream RIPK3 activation. The gene discussed is CASP8; the disease is infection.