This aligns with existing studies highlighting the role of hypoxia and, by extension, the HIF‐1 signaling pathway in enhancing RANKL‐induced osteoclast formation,[48, 49] whereas hyperoxic conditions have been shown to inhibit this process.[50, 51] Furthermore, analysis of cis‐acting expression quantitative trait loci in patients with rheumatoid arthritis revealed a correlation between higher HIF‐1α expression and increased bone erosion,[52] underscoring the clinical relevance of HIF‐1 signaling in bone pathology. Here, TNFSF11 is linked to rheumatoid arthritis.