These two intronic SNPs were not in linkage disequilibrium (LD) with any of the protein-coding variants of PLB1 (r2<0.3 for common variants [MAF ≥0.05] and r2<0.1 for low-frequency or rare variants [MAF<0.05]), suggesting that observed RA risk was primarily derived from non-coding variants of PLB1. The gene discussed is PLB1; the disease is rheumatoid arthritis.