A prototypical example is SpA, a highly TNF blockade–responsive form of chronic inflammatory arthritis that displays a set of unique characteristics such as spinal involvement, tendinitis, osteitis, and extensive new bone formation that are not recapitulated in the commonly used TNF overexpression models (Dougados and Baeten, 2011; Vieira-Sousa et al., 2015). The gene discussed is TNF; the disease is bone inflammation disease.