The conversion of microglia and astrocytes that are physiologically essential for healthy neuronal function into a pathologically activated state that negatively impacts motor neuron function and survival is well recognized as an important feature of ALS.34 Here, we show that in contrast to the ALS model SOD1G37R mice that show a gene expression signature for deleterious activation of microglia and astrocytes in the affected spinal cord, Slc31a1+/− mice do not provide clear evidence for aberrant glial activation (Fig. 4). Here, SLC31A1 is linked to amyotrophic lateral sclerosis.