First, the main pathogens detected in pleural infections (the Streptococcus milleri group, Staphylococcus aureus, Streptococcus pneumoniae) encode DNases in their genomes. Those nucleases are emerging as potential virulence factors, due to their ability to degrade neutrophil extracellular traps (NETs).3 Released from neutrophils, NETs, composed mainly of chromatin and certain proteins, entrap and kill bacteria extracellularly. Furthermore, those weblike structures are in abundance in pus,4 thus, their disassembly may explain the appreciable viscosity reduction after DNase treatment. Another issue is the DNases’ biofilm-dispersing activity. Indeed, DNases have been reported to degrade biofilms,5 but their role in acute infections is an open question. To refine our therapeutic strategies, the exact nature of the tissue plasminogen activator-DNase synergism and NETs disruption impact on clinical course are areas in which further insight must be gained.