Originally, IBM was considered to be a cytotoxic T cell-mediated disease with no humoral autoimmunity, until the finding of immunoglobulin transcripts in IBM muscle samples, and the finding of a 43-kD autoantibody, identified as being directed to cytosolic 5-nucleotidase 1A (anti-NT5c1A or anti-cN1A) [9,103,104]. This evidence concerns the gene NT5C1A and inclusion body myositis.