A recent analysis of a mouse model of arthritis-associated scleritis revealed that macrophages, plasma cells, and deposition of immune complexes jointly participate in the pathogenesis of scleritis [44], and suggested targeting molecular targets, such as TNF-α and IL-6, inhibiting macrophage activity, and CD20, suppressing antibody-producing cells, instead of targeting T-cells. The gene discussed is TNF; the disease is scleritis.