Mice carrying an inactivating -mutation in the proline-serine-threonine phosphatase-interacting protein 2 gene (Pstpip2) develop a phenotype reminiscent of CRMO, which is associated with over-production of IL-1β, enhanced osteoclastogenesis and bone resorption, responses that depend on IL-1 receptor and IL-1β, but not IL-1α, and are driven by neutrophils [21, 22]. This evidence concerns the gene PSTPIP2 and chronic recurrent multifocal osteomyelitis.