While the ΔE mutation impairs the ability of torsinA to interact with or be stimulated by either LAP1 or LULL1 (Naismith et al., 2009; Zhao et al., 2013), a mechanistic understanding of how the ΔE mutation drives DYT1 dystonia pathogenesis at the cellular level remains unclear. The gene discussed is TOR1A; the disease is early-onset generalized limb-onset dystonia.