In multiple myeloma (in vivo model), the loss of ALCAM was seen together with increased survival, reduced osteolytic lesions, and changed bone modelling, an event thought to be due to ALCAM-mediated osteoclastogenesis via an altered balance of RANKL (receptor activator of nuclear factor kappa-B ligand) and osteoprotegerin [108]. The gene discussed is ALCAM; the disease is plasma cell myeloma.