Notwithstanding these limitations, the strengths of the current study—in which novel immunological observations from our highly translational murine model of HRS-induced myositis are merged with shifts in the clinical phenotype of humans with Jo-1 antibody-positive anti-synthetase syndrome–provide ample rationale for future studies exploring the clinical implications of anti-Ro52 and anti-Ro60 autoimmunity in IIM. Here, TRIM21 is linked to myositis disease.