Previous studies have reported the altered expression of CD57 and KLRG1 on CD4+ and γδ T cells in chronic inflammatory conditions such as cancer, autoimmune diseases and viral infections (32–36), however, it remains to be determined whether the phenotype changes observed in CD8+ T-LGL extend to other T cell subsets and contribute to the overall immune dysregulation in IBM. This evidence concerns the gene CD4 and inclusion body myositis.