In order to eliminate the possibility that this clusterin upregulation was simply a response to any cellular stressor present in AD, we treated OPCs with other factors known to be upregulated in Alzheimer’s disease, including TNFα, IFNγ, and reactive oxygen species (ROS), which all failed to produce any change in clusterin expression (Fig. 2I–J)[27–29]. The gene discussed is CLU; the disease is Alzheimer disease.