TNFSF11 and neoplasm: Future studies should incorporate functional validation, including lineage or fate-mapping approaches to clarify CAF origin and persistence within OSCC lesions, systematic cytokine/chemokine profiling to identify mediators of CAF–osteoclast crosstalk (e.g., RANKL/OPG axis), and targeted perturbation of CAF–tumor or CAF–osteoclast signaling to test necessity and sufficiency for bone destruction [3,11].