Streptococcus pyogenes (Group A Streptococcus, GAS) is an enigmatic human-restricted pathobiont, capable of both colonization and infection. Illnesses range in severity from superficial to invasive disease. GAS is also the causative agent of non-suppurative sequelae including acute rheumatic fever (ARF) and rheumatic heart disease (RHD), both significant global sources of morbidity and mortality. While historically it has been thought that GAS pharyngitis leads to ARF/RFH, current data better support the hypothesis that superficial skin infections (e.g. impetigo or cellulitis) are incipient to ARF/RHD, making it critical to understand mechanisms of skin infection. We have developed and validated a murine model mimicking early stages of GAS skin infection. Using RNA sequencing, we have identified genes critical for skin infection, including an intriguing proposed dual-acting small RNA (sr0235) and peptide (0235c) pair that is significantly upregulated during skin infection. In this pair, a proposed sRNA encompasses a standalone open reading frame and promoter. In silico analysis of this locus suggests that the pair are involved in zinc homeostasis and finds broad conservation across GAS and Streptococcus agalactiae. In vitro studies demonstrate that absence of this pair impair growth under zinc-limited conditions, with peptide expression induced during zinc chelation. While additional studies are pending to tease apart the unique functions of the peptide and sRNA, these results have led to the hypothesis that that this sRNA/peptide pair play a critical role in infecting zinc-poor epithelial surfaces and may allow us to detangle critical early interactions leading to skin infections.