CD8A and inclusion body myositis: IBM pathogenesis centrally involves cytotoxic, senescent CD8+ T cells, defects of autophagy and ubiquitin–proteasome system (UPS) resulting in proteostasis impairment and abnormal sarcoplasmic protein aggregation, along with endoplasmic reticulum and mitochondrial alterations, and antibodies to the cytosolic 5′-nucleotidase 1A (anti-cN1A) [1, 5].