Given that synovial fibroblasts are recognized as key pathogenic cells in RA—capable of driving synovitis and tissue destruction through the secretion of chemokines, matrix-degrading enzymes, and inflammatory mediators (32, 33)—the enrichment of CHI3L1 in this cell population suggests a pivotal role in shaping the local microenvironment. The gene discussed is CHI3L1; the disease is rheumatoid arthritis.