Systemic assessment indicated a predominantly ASyS-driven phenotype: although ESSDAI was moderately elevated (median 15, IQR 7.5-21), the adapted ESSDAI markedly decreased (median 5, IQR 0-6.5), reflecting limited SjD-specific systemic activity.<h4>Conclusions</h4>The SjD-ASyS overlap seem characterized by a coherent clinical-serological phenotype, defined by anti-Ro52-positive sicca presentation, non-Jo1 anti-ARS autoantibodies and early interstitial lung disease. The gene discussed is TRIM21; the disease is interstitial lung disease.