The fact that under- or over-expression of dATP7 and over-expression of either wildtype or M1311V hATP7A all induced similar locomotor deficits reminiscent of TDP-43 based models of ALS (Estes et al., 2011) in Drosophila larvae highlights the important role that precise regulation of ATP7A expression and, consequentially, copper homeostasis, plays in maintaining motor function. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.