While in murine CMV model and WNV infection model, TNFα antagonist indeed rectified cerebellar abnormalities and developmental gene expression, it has been found to augment Multiple Sclerosis phenotype in humans by increasing peripheral and CNS autoimmunity (Sicotte and Voskuhl, 2001; Shrestha et al., 2008). The gene discussed is TNF; the disease is Autoimmunity.