Our findings on the role of the Hla-ADAM10 interaction in endothelial injury (10, 12), together with the observation that a SNP in the ADAM10 promoter influences the outcome of human bacterial sepsis (32), led us to hypothesize that endothelial injury by Hla may initiate the series of events that culminate in S. aureus sepsis–associated microvascular thrombosis. The gene discussed is ADAM10; the disease is bacterial infectious disease with sepsis.