The mutation rescues dauer formation defects seen in mutants.

Collapsin response mediator protein-2 (CRMP2) in humans, UNC-33 in , is a molecule that mediates axonal outgrowth and stability. UNC-33/CRMP2 has been hypothesized as a potential drug target for treating Alzheimer's and other neurodegenerative diseases, which can often be attributed in part to aging. In aging, CRMP2 becomes hyperphosphorylated, which decreases the protein's functionality, destabilizes the cellular skeleton, and contributes to neurodegeneration.