Our analysis of lung transcriptomics did suggest a potential early lung enrichment of neutrophiles in response to H9N2 infection, evidenced by CXCR2, the main receptor mediating the lung migration of neutrophils during influenza infection, and three major neutrophil-attracting chemokines, namely CCL3, CXCL-1, and CXCL2, which all exhibited a pattern consistent with an early induction by H9N2 infection compared to H7N9 infection (data not shown). The gene discussed is CXCL1; the disease is influenza.