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Based on an increasing understanding of the complexity of regulating host cell necrosis in COVID-19 and the connection with the intrinsic immune defense mechanism of SARS-CoV-2 infection (innate immunity of cells), we speculate that regulated necrosis plays a double-edged sword role in COVID-19 and seems to depend on many factors, including downstream effector molecules (various cytokines and chemokines), the specific cell death pathway involved, and the immune response at different clinical stages of COVID-19 progression