Other cell types also respond to ALS pathology in mouse models and human patients, but do not degenerate.10,11 For instance, the sciatic nerve consists of axons extending from spinal motor neurons and sensory dorsal root ganglion (DRG) neurons, and in sciatic nerves of ALS model mice, hyper-activated macrophages cause the selective degeneration of spinal motor neurons.12 However, both motor and DRG neurons in ALS accumulate mutant SOD1, an ALS-associated protein,13 suggesting a similar protein homeostatic stress burden. Here, SOD1 is linked to amyotrophic lateral sclerosis.