The most prominent mechanistic hypothesis for IBM myodegeneration implicates abnormal proteostasis, as many proteins associated with neurodegenerative disease (e.g. TDP-43, p62, amyloid-β, and αβ-crystallin) are reported to aggregate in the cytosol of IBM-affected myofibers [2, 12, 23]. This evidence concerns the gene TARDBP and inclusion body myositis.