In addition, acm [26], efaA [27], ebp [28], and gls24 [29] are involved in the pathogenesis of endocarditis; scm has a high prevalence in clinically related E. faecium [30]; sgrA and ecbA are the marker for clinically associated E. faecium [31]; bopD contributes to prolonged mouse bacteremia [32]; prpA is proposed to contribute to colonization and infection, and its N-terminus is able to bind to fibrinogen, fibronectin and platelets [33]; cad contributes to facilitating conjugation, chemotactic for human neutrophils [34]. This evidence concerns the gene CAD and endocarditis.