Other studies focused their attention on recapitulating the cytoplasmic accumulation of TDP-43, demonstrating that overexpression of either the full length wild type protein (Johnson et al., 2008; Li et al., 2010; Liachko et al., 2010; Tsai et al., 2010; Wils et al., 2010; Igaz et al., 2011) or a disease-associated variant (Kabashi et al., 2009; Wegorzewska et al., 2009; Liachko et al., 2010; Zhou et al., 2010; Estes et al., 2011; Huang et al., 2012), is sufficient to cause ALS phenotypes in various animal models. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.