The molecular and cellular mechanisms of abnormal orbital tissue remodeling in GO involve the activation of orbital fibroblasts, leading to orbital myofibroblast differentiation, activation of T helper cells including Th1, Th2, and Th17 cells, increased secretion of inflammatory cytokines such as IFN-γ, TNF-α, interleukins, and prostaglandin E2, as well as hyaluronan production and deposition in the extracellular matrix (ECM), and adipogenesis [3]. This evidence concerns the gene TNF and geroderma osteodysplastica.