In line with the present findings, which showed that overexpressing PHB2 is an effective way to reduce myocardial inflammation and normalize heart performance under endotoxemia conditions, evidence from rodent models of arthritis 63, spondylarthropathies 64, ulcerative colitis 65, and endotoxin-mediated acute lung injury 66 highlighted also the functional importance of PHB2 in neutralizing abnormal inflammatory responses. This evidence concerns the gene PHB2 and spondyloarthropathy.