A substantial body of work has demonstrated that astrocytes are involved in ALS pathogenesis (Ilieva et al., 2009; Yamanaka and Komine, 2018), both via loss of critically important functions such as extracellular glutamate uptake (Rothstein et al., 1995) and toxic gain-of-function such as altered transforming growth factor β (TGFβ) signaling (Phatnani et al., 2013) and increased production of reactive oxygen species (ROS) (Cassina et al., 2008). The gene discussed is TGFB1; the disease is amyotrophic lateral sclerosis.