Consistent with its immunomodulatory role, we found that the pretreatment with rhLAV-BPIFB4 (18 ng/mL) significantly reduced MCP-1 release (790 ± 124 pg/mL vs 1989 ± 456 pg/mL; p = .011), which is responsible for abundant inflammatory cell infiltration to sites of infection in vivo. The gene discussed is BPIFB4; the disease is infection.