Bryant et al. (2003) reported that heat-killed S. pyogenes bacteria of serotypes M1 and M3, but not M6, have the ability to stimulate TF and cytokine induction in endothelial cells and monocytes. Our findings that M1 protein alone induces TF-expression in monocytes support these data and show an important role for M proteins in coagulation disorders. Moreover, our data show that S. pyogenes bacteria have developed a mechanism that evokes coagulation dysfunction that is not restricted to the site of infection and may result in a systemic activation of the coagulation system. This evidence concerns the gene MYOM2 and blood coagulation disease.