However, silencing PHLDA3 expression in human SOD1 ALS spinal astrocytes and even in control astrocytes characterized by lower levels could prevent sodium arsenite (SA)-induced oxidative stress in spinal neurons, measured by the formation of Ras GTPase-activating protein (GAP)-binding protein-1-positive (G3BP1+) stress granules (SGs). Here, PHLDA3 is linked to amyotrophic lateral sclerosis.