In a chronic model of MS, there is a decrease in NSC self-renewal in the SVZ (Pluchino et al., 2008) that is spatiotemporally correlated with increase in Stat1. To determine whether STAT1 plays a causative role in regulating self-renewal in NSCs, we delivered STAT1 to wild type NSCs isolated from the SVZ using a bicistronic retroviral vector LTR-STAT1-IRES-GFP containing the coding sequence of Stat1 and GFP (Lesinski et al., 2003). The gene discussed is STAT1; the disease is myeloid sarcoma.