In a 2011 research article, Voskuhl published data revealing that the estrogen receptor α (ERα) on astrocytes, not neurons, was responsible for the reduction of clinical EAE symptoms in mice. Using a gene knockout system Cre-Lox, the research team was able to remove ERα from neurons and in separate mice, remove ERα from astrocytes. It was found that the mice with ERα knocked out in astrocytes experienced an increase in clinical disease symptoms, macrophage and T-cell inflammation in the central nervous system, and axonal loss.