Its secretion of epidermal exfoliative toxins (ExhA, ExhB, ExhC, ExhD, ShetA, and ShetB) acts specifically on desmoglein 1 (Dsg1) to cause separation of keratinocytes, resulting in blistering of the skin to form dermatitis, which is in line with the mechanism of staphylococcal scalded skin syndrome (SSSS) caused by the exfoliative toxins (ETA, ETB and ETD) of S. aureus [6,7,8]. This evidence concerns the gene EDNRB and staphylococcal scalded skin syndrome.