Juvenile Idiopathic Arthritis (JIA) is an inflammatory disorder characterized by swelling of one or more joints, and usually has a significant impact on a child’s mobility and quality of life. Accumulating evidence suggests that neutrophils (N?) make an important contribution to the recruitment and activation of innate immune cells, thereby amplifying the inflammatory response and contributing to pain and joint injury in JIA. The long term goal is to identify signaling pathways modulating neutrophil activation during JIA. Recruitment and adhesion of neutrophils to the inflamed joints and activation of the transcription factor NF-?B are two major pathways modulating neutrophil’s release of inflammatory cytokines. Considering the possible side effects of NF-?B inhibition due to its global expression, it becomes crucial to identify the details of NF-?B activation in neutrophils. Dr. Faccio and her collaborators have found that PLC?2, a phospholipase controlling integrin-mediated adhesion, modulates NF-?B activation and the development of the neutrophil response in murine inflammatory arthritis. Examining the details of this novel ß2 integrin/ PLC?2/ NF-?B pathway and identifying NF-?B target genes upon cell attachment might provide new insights into mechanisms of neutrophil activation during arthritis that may lead to more specific therapeutic strategies for the treatment of JIA.