A previous study indicated that YY1 promoted NF‐κB‐mediated overexpression of inflammatory cytokines in rheumatoid arthritis.[69] Moreover, YY1 affected Th17 cell activation and positively regulated the STAT3 pathway.[70] Concurrently, emerging research on epigenetic modifications of YY1 includes YY1 phosphorylation at S118, which contributes to atherosclerosis, and YY1 deacetylation, implicated in renal fibrosis.[36, 71] Despite AU being a prototypical inflammatory condition necessitating novel treatments, no studies have linked AU with YY1 lactylation. This evidence concerns the gene STAT3 and rheumatoid arthritis.