The characterization of T and B cell populations in inflammatory infiltrates, the discovery of myositis-specific autoantibodies (MSA) and myositis-associated autoantibodies (MAA) with corresponding clinical phenotypes, and new insights into the role of derangements of the complement system and the important contribution of interferonopathy have led to increased understanding and new targets for therapy. This evidence concerns the gene NAA10 and myositis disease.