McLoughlin et al. (2017) used fluorescein isothiocyanate-labeled dextran (40 kDa) to demonstrate that S. aureus infection can enhance the permeability of the BBB by decreasing vascular endothelial cadherin, claudin-5, and zonula occludens-1 levels in a dose-dependent manner. Moreover, Baldwin and Kielian (2004) reported that in the murine BA model, staphylococcal BA development results in the persistent opening of the BBB. This effect may favor the distribution of antibody drugs to the central nervous system. The S. aureus factors that participate in BBB opening warrant further investigation. Here, CLDN5 is linked to breast angiosarcoma.