Recent evidence demonstrates that dysregulated chemokine–receptor interactions, including CCL2/CCR2, CCL5/CCR5, and CX3CL1/CX3CR1, disrupt the equilibrium between osteogenesis and osteoclastogenesis, thereby contributing to the pathogenesis of osteoporosis, osteoarthritis, multiple myeloma, and bone metastasis. This evidence concerns the gene CCL5 and AL amyloidosis.