Our speculation that extraneous Z-NA induces Zαβ dimerization, creating a platform for ZBP1 self-aggregation and cross-polymerization with other proteins (e.g., RIPK1 and RIPK3) through their RHIM domains, offers insights into the potential of ZBP1 to orchestrate an immune response tailored to various pathogenic infections, while simultaneously averting excessive autoimmune reactions. The gene discussed is RIPK3; the disease is infection.