This process involves the receptor activator of nuclear factor‐κB ligand (RANKL), which induces osteoclastogenesis, leading to osteoclastic bone destruction, and enzymatic cartilage degradation.[1, 4] FLSs have emerged as a therapeutic target in RA to avoid side effects such as systemic immune suppression associated with many current RA treatments.[5] However, therapeutic options that specifically and directly target RA‐FLSs in individuals with RA are still lacking. The gene discussed is TNFSF11; the disease is rheumatoid arthritis.