Based on the somewhat unexpected findings in our mouse model of HRS-induced myositis (most notably the development of anti-Ro60 antibodies), we sought to determine associations between the presence of anti-Ro52 and/or anti-Ro60 antibodies and the clinical phenotype of anti-Jo-1 (HRS) antibody-positive patients with the anti-synthetase or other overlap syndromes. This evidence concerns the gene TRIM21 and myositis disease.