We read the article by Hsu et al. (2011) with great interest. The authors have convincingly demonstrated that bacterial autolysis, and extracellular DNA (e-DNA) thereby released, contributes to the enhanced biofilm-formation by vancomycin nonsusceptible Staphylococcus aureus (VNSSA) upon exposure to sublethal vancomycin concentration. Many previous publications have also reported an increased biofilm-formation by staphylococci upon exposure to vancomycin (Dunne, 1990; Cargill & Upton, 2009; Kaplan et al. , 2011; Mirani & Jamil, 2011). The majority of these articles have focused on vancomycin-susceptible strains, and studies specifically targeting VNSSA biofilms (Mirani & Jamil, 2011) are rare. Also, most studies have linked the antibiotic-enhanced Staphylococcus biofilm-formation (especially Staphylococcus epidermidis ) to an increased production of polysaccharide intercellular adhesin (PIA), the principal component of biofilm matrix, perhaps via down-regulation of PIA repressor TcaR (Rachid et al. , 2000; Chang et al. , 2011). Interestingly, Hsu et al. (2011) demonstrate a role of e-DNA for this mechanism in VNSSA. Although the production of PIA was increased upon exposure to sublethal vancomycin in one strain (SJC1200), e-DNA played a more important role, with DNase significantly reducing vancomycin-enhanced biofilm-formation to levels similar to untreated cultures in both the strains tested (SJC1200 and Mu50) and xenogenic DNA promoting biofilm development. These findings add considerably to the currently available literature on S. aureus biofilms and perhaps correlate with a greater role of e-DNA, rather than PIA, in S. aureus biofilm development (Izano et al. , 2008). Another study has also implicated both PIA and e-DNA for antibiotic-augmented biofilm-formation, depending upon strain or drug tested, albeit in vancomycin-susceptible S. …