These effects are further augmented by the increased expression of adhesion molecules on the endothelium of the BBB in SLE which enhances adhesion and subsequent penetration of neutrophils into the CNS, with neutrophil products including MMP-9 and reactive oxygen species compounding BBB dysfunction and permeability to other inflammatory insults (Figure 1). The gene discussed is MMP9; the disease is systemic lupus erythematosus.