Therefore, we supposed that in the pathogenesis of GO, when Th17 cells are stimulated by ROS, IL-17A is released to activate the orbital fibroblasts, by which NLRP3 inflammasomes are activated, with caspase-1 further promoting fibroblasts to secrete IL-1β to form a subsequent immune inflammatory response. This evidence concerns the gene NLRP3 and geroderma osteodysplastica.