For example, flavivirus proteases disrupt the cGAS–STING pathway by cleaving human cGAS and STING,[38] while picornavirus 3C proteases directly cleave key adaptors MAVS and TRIF to inhibit RLR/TLR‐mediated interferon production.[39] In striking contrast, our knowledge of host‐encoded proteases that directly target and cleave viral proteins to restrict infection remains notably limited.[40] Our findings reveal an evolutionary counter strategy where host lysozymes have been repurposed as antiviral proteases. The gene discussed is MAVS; the disease is infection.