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We report that in GAS,<jats:italic>stk<\/jats:italic>is required to produce disease in a murine myositis model of infection. Using microarray and quantitative reverse transcription-PCR (qRT-PCR) studies, we found that Stk activates genes for virulence factors, osmoregulation, metabolism of \u03b1-glucans, and fatty acid biosynthesis, as well as genes affecting cell wall synthesis. Confirming these transcription studies, we determined that the<jats:italic>stk<\/jats:italic>deletion mutant is more sensitive to osmotic stress and to penicillin than the wild type. 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