Specifically, mutation of atl and pbp3 has been shown to limit septic implant loosening and abscess formation in the medullary cavity, while mutation of pbp3 has been correlated with reduced peri-implant osteolysis, reduced osteoclast activity, reduced invasion of the OLCN, and reduced production of the activator of nuclear factor kappa-B ligand (RANKL), a central modulator of the balance between osteoblast and osteoclast activity in bone remodeling [34,46]. The gene discussed is TNFSF11; the disease is abscess.