Loss of ulp-3(tm1287), whose human homolog NEDP1 regulates stress granule dynamics, reduces the formation of stress granules and rescues SOD-1(G85R) motor deficits, indicating stress granule formation may facilitate ALS-related neuron dysfunction (Table 2) (Kassouf et al., 2023). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.