Specifically, preclinical studies using models of SpA have shown that expression of genes encoding proinflammatory cytokines including interleukin (IL)-17A, tumor necrosis factor (TNF)-α, and IL-23 is upregulated in affected joints [9, 13] and that IL-17 promotes osteogenesis at inflamed sites (e.g., entheses) under conditions of mechanical stress, resulting in excess bone formation that is a key characteristic difference between SpA and rheumatoid arthritis (RA), which is characterized predominantly by bone erosion and resorption [14]. Here, IL17A is linked to rheumatoid arthritis.