To measure the impact of HMGB1-RAGE signaling on vascular permeability, HUVEC monolayers grown on 8 μm Transwell chambers were stimulated with CMs from uninfected or oHSV-infected glioma cells in the presence or absence of a RAGE-blocking antibody (2 μg/mL) or purified esRAGE (200 ng/mL), and the amount of Evan’s Blue albumin (EBA) that permeated the monolayer to the lower chamber was measured to evaluate vascular leakiness (Figure 2B). The gene discussed is AGER; the disease is glioma.