We also found that silencing of Gls2 significantly reduced transcription of IL-1β, an important part of the innate immune response to S. aureus. IL-1β is required for both neutrophil recruitment [12] and regulation of pro-inflammatory Th17 response to S. aureus [36], and is sufficient for abscess formation in immunity against S. aureus in mice [37]. This evidence concerns the gene GLS2 and abscess.