Importantly, we found that both necroptosis inducer TSZ treatment and overexpression of RIPK3 and MLKL significantly inhibited CSFV replication and infection progression, whereas the necroptosis executioner MLKL clearly promoted CSFV replication when inhibited by NSA, suggesting that necroptosis is a limiting host factor for CSFV infection and that CSFV infection-induced autophagy disintegrates this host defense mechanism to promote its sustained replication. The gene discussed is RIPK3; the disease is infection.