In line with this, it was recently shown using a Drosophila OPMD model that increased proteasome activity arises during OPMD progression, potentially in part through proteasome plugging with mutant PABPN1 oligomers, leading to muscle atrophy by degradation of myofibrillar proteins [33]. The gene discussed is PABPN1; the disease is oculopharyngeal muscular dystrophy.