Furthermore, Scianaro et al. [45] suggested increased NLRP3 inflammasome activation contributing to the inflammatory phenotype in CRMO, showing increased mRNA expression of inflammasome components (ASC, NLRP3, caspase-1) as well as increased IL-1β transcription and release from peripheral blood mononuclear cells from active CRMO patients compared to patients with inactive disease and controls after stimulation with LPS. This evidence concerns the gene IL1B and chronic recurrent multifocal osteomyelitis.