The irr-deficient strain was more susceptible than wild-type to killing by H2O2 across a range of different concentrations, and was hypersensitive to killing by the cell envelope active antimicrobial peptides LL-37 and cathepsin G. Inactivation of irr delayed the formation of skin abscesses and resulted in smaller abscesses, indicating that Irr is required for full GAS virulence in a mouse model of subcutaneous infection. This evidence concerns the gene INSRR and Cutaneous abscess.