Numerous myositis-specific autoantigens have been described, including the signal recognition particle (SRP), the helicase Mi-2, and a battery of aminoacyl tRNA synthetases (e.g., histidyl [Jo-1], threonyl [PL-7], alanyl [PL-12], isoleucyl [OJ], glycyl [EJ]), and autoantibodies directed against each are thought to define distinct myositis syndromes: antisynthetase syndrome, for instance, is strongly associated with interstitial lung disease, while Mi-2 autoantibodies are thought to confer reduced risk for a myositis-associated malignancy [10]. This evidence concerns the gene UCN2 and antisynthetase syndrome.