IL‐9 expression, which is persistently high in patients with R527C‐associated MAD (Figure 1D), has been shown to promote osteoclast formation in rheumatoid arthritis.[39] Furthermore, IL‐6 has been shown to activate osteoclastogenesis by regulating RANKL via the JAK‐STAT3 pathway,[40] suggesting IL‐6 inhibitors as potential therapeutics for reducing bone resorption in MAD. Here, TNFSF11 is linked to rheumatoid arthritis.