This aligns with previous findings in China and reflects the relatively low prevalence of SE positivity in the Chinese RA population.[25] Prior research has suggested that HLA-DRB1*04:05 may drive joint destruction by modulating the Th17/Treg balance rather than simply influencing ACPA production.[26] This insight provides a novel perspective for understanding the clinical heterogeneity of RA. This evidence concerns the gene HLA-DRB1 and rheumatoid arthritis.