This phenotype is further supported by findings from the Chinese SLE Treatment and Research Group (CSTAR) registry, in which both anti-SSA positivity and older age at onset independently predicted organ damage accumulation in SLE patients.[30] These results suggest that Cluster 2 represents a high-risk subgroup within late-onset SLE, necessitating vigilant monitoring for progressive organ damage—particularly cardiopulmonary complications. The gene discussed is TRIM21; the disease is systemic lupus erythematosus.