PTPRB and infection: Our findings, presented here and elsewhere [8], demonstrate that the deletion of ptpB in the clinical S. aureus isolate SA564 alters the transcription of various genes/operons whose products are involved in stress adaptation and infectivity, suggesting that PtpB-driven removal of phosphates from arginine phosphosites is another posttranscriptional mechanism utilized by this pathogen to fine-tune the expression and activity of its virulon, in order to successfully adapt to the diverse host environmental conditions encountered by the bacterium during infection.