The article discusses the role of *Staphylococcus aureus* in causing food poisoning, focusing on the production and effects of staphylococcal enterotoxins (SEs). SEs are potent gastrointestinal exotoxins produced by *S. aureus* and are responsible for the rapid onset of symptoms such as nausea, vomiting, and abdominal cramping. The toxins are resistant to heat and proteolytic enzymes, allowing them to survive in the digestive tract. SEs are classified into classical (SEA to SEE) and new types (SEG to SE/U2), with all possessing superantigenic activity. The article highlights that SEA is the most common cause of staphylococcal food poisoning worldwide, while other classical SEs and new SEs like SEH have also been implicated. The toxins are encoded by accessory genetic elements, including plasmids, prophages, pathogenicity islands, and genomic islands. The article also discusses the structure and mode of action of SEs, emphasizing their interaction with MHC class II molecules and T-cell receptors, and their ability to stimulate the vagus nerve and activate immune responses. The presence of SE genes in various genetic elements and their role in food poisoning outbreaks is explored, with SEA being the most frequently detected toxin in outbreaks. The article concludes by noting the ongoing research into the pathogenicity of SEs and the need for further understanding of their mechanisms of action.The article discusses the role of *Staphylococcus aureus* in causing food poisoning, focusing on the production and effects of staphylococcal enterotoxins (SEs). SEs are potent gastrointestinal exotoxins produced by *S. aureus* and are responsible for the rapid onset of symptoms such as nausea, vomiting, and abdominal cramping. The toxins are resistant to heat and proteolytic enzymes, allowing them to survive in the digestive tract. SEs are classified into classical (SEA to SEE) and new types (SEG to SE/U2), with all possessing superantigenic activity. The article highlights that SEA is the most common cause of staphylococcal food poisoning worldwide, while other classical SEs and new SEs like SEH have also been implicated. The toxins are encoded by accessory genetic elements, including plasmids, prophages, pathogenicity islands, and genomic islands. The article also discusses the structure and mode of action of SEs, emphasizing their interaction with MHC class II molecules and T-cell receptors, and their ability to stimulate the vagus nerve and activate immune responses. The presence of SE genes in various genetic elements and their role in food poisoning outbreaks is explored, with SEA being the most frequently detected toxin in outbreaks. The article concludes by noting the ongoing research into the pathogenicity of SEs and the need for further understanding of their mechanisms of action.