In non-neoplastic conditions, like Streptococcus pneumoniae infection in mice, neutrophil IFN-γ production is under control of toll-like receptor engagement via MYD88, but not the CD11b/CD18 complex, and induces transcription of target genes (members of nonreceptor Src kinase family, Hck, Fgr, and Lyn), which are critical for the acute inflammatory response and initiation of immune response [35]. This evidence concerns the gene ITGAM and pneumococcal infection.