The findings that clinical isolates of skin and mucosal origin expressing high levels of SAK show a more efficient invasion of internal organs than strains expressing a low level of SAK, and the finding that in animal sepsis wild type strains show an increased bacterial load compared to the sak isogenic mutants (Bokarewa et al., 2006) supports evidence that SAK is an important staphylococcal virulence factor. This evidence concerns the gene PLK4 and Sepsis.