TNFSF11 and neoplasm: The molecular mechanisms by which tumor-specific αvβ3 promotes osteolysis are still being explored, but prior studies have shown that αvβ3 signaling resulted in the nuclear localization of transcription factors such as Runx2, which upregulated matrix metalloproteinases (e.g., MMP-9, MMP-13) and soluble receptor activator of NF-κB ligand (RANKL) to aid in bone matrix dissolution as well as osteoclast recruitment, differentiation, and function [37,38].