The damage-based mechanism of necrosis in skeletal muscle tissue is characterized by an upregulation of HLA-ABC on muscle fibers that prompted those fibers to be recognized by CD8+ T cells, which attack and invade the HLA-ABC+ muscle fibers in DM patients25, by releasing several mediators such as granzyme-B and perforin-152. The gene discussed is GZMB; the disease is dermatomyositis.