However, despite the marked regenerative process, our IBM muscles do not express greater levels of DM-specific pathological isoforms of the muscle-specific genes than those observed in CTR, except for RYR1. The altered splicing of RYR1 could explain the recent data by Amici et al. (55) who reported a lower protein expression of RyR1 in IBM muscles as compared to healthy subjects, indicating that Ca2+ dysregulation may contribute to muscle weakness and atrophy in this myopathy. The gene discussed is RYR1; the disease is inclusion body myositis.