Nevertheless, similar to many of the themes of pathogenesis of Lafora disease, the proteomic data reported here reveal striking differential expression between APBD subjects and controls of many proteins, pathways and protein–protein networks related to the unfolded protein response, endoplasmic reticulum stress pathway, ubiquitinylation, mTOR signaling, and apoptosis. The gene discussed is MTOR; the disease is adult polyglucosan body disease.