Therapeutic targets for neurodegenerative conditions are constantly emerging. Diseases such as amyotrophic lateral sclerosis and Huntington's disease are multifactorial and involve dysfunction of various cellular pathways. Protein aggregate formation is one of the crucial pathological signs of cellular dysfunction, and is characteristic of many neurodegenerative conditions. Proteins recruited to these aggregates are thought to play a role in formation of the pathogenic inclusions. This review aims at exploring the current evidence for protein aggregation and the role for Arfaptin2, as a candidate factor contributing to the formation of aggresomes and a potential therapeutic target in motor neuron disease.