As mentioned by Andia and Maffulli [53], the current in vitro systems of joint disease are not able to address the role of the immunologic system, notably the macrophage activity induced by proteins of the group-specific component globulin that activates these cells via the innate immune toll-like receptor 4 and induces the expression of TNF-α, IL-1β, IL-6, and vascular endothelial growth factor. This evidence concerns the gene IL1B and arthropathy.