PRTN3 and rheumatoid arthritis: Although the detailed pathogenesis of RA is still unclear, genetic factors, aberrant autoimmune antibodies (rheumatoid factor (RF), anti-cyclic citrullinated peptide antibody (ACPA), etc.), dysregulated immune cells (such as B cells, CD4+ T cells, etc.), and excessive systemic inflammation contribute to RA development and progression (6–8).