In human M-Mφ or GM-Mφ, we demonstrated that knocking down CLEC5A expression by gene silencing, blocking influenza-CLEC5A interactions with anti-CLEC5A antibodies, or dampening CLEC5A-mediated signaling using a Syk inhibitor consistently reduced levels of proinflammatory cytokines without affecting the replication of influenza viruses of different subtypes. The gene discussed is SYK; the disease is influenza.