In short, the pathogenicity of at least some myositis-specific autoantibodies is plausible, as supported by the finding of related auto-antigen overexpression in IIM patients (e.g., TIF1-γ overexpression in endometrial cancer cells in patients with cancer-associated DM with anti-TIF1-γ autoantibodies) and experimental passive immunization via auto-antibody transfer (in in vitro and in vivo models of seropositive IMNM) [26,55,56,57,58]. This evidence concerns the gene TRIM33 and dermatomyositis.