We found that IFN-γ-deficient mice treated with the antibiotic ceftriaxone survived pneumococcal meningitis with reduced cognitive and behavioral disorders compared to their wild-type counterparts and that the nexus between the toll-like receptors (TLRs) 2 and 4, IFN-γ and the enzyme indoleamine 2,3-dioxygenase-1 contributed, at least in part, to the neurological sequelae resulting from pneumococcal meningitis (Too et al., 2014; Too and Mitchell, 2021). This evidence concerns the gene IFNG and pneumococcal meningitis.