In Inclusion Body myositis, it has been proposed that CD8+ terminally differentiated memory effector (TEMRA) T cells are involved in the pathophysiology of the disease through mechanisms involving cytotoxic enzymes (perforin and granzyme) as well as being mediated by IFN-γ, leading to an increase in the expression of HLA class I molecules, endoplasmic reticulum stress and proteasome dysfunction, with a consequent induction of rimmed vacuole formation and degenerative features (Arahata and Engel, 1984). The gene discussed is CD8A; the disease is inclusion body myositis.