ANXA2 has been reported as an oxidative stress signal for Vδ2−γδ T cells.[25] Furthermore, thyroid hormone synthesis generates reactive oxygen species (ROS), establishing a high‐ROS intracellular milieu.[68] These clues collectively point to stress surveillance—where stressors (e.g., infection, psychological stress) exacerbate oxidative stress, overwhelming antioxidant defenses and damaging TFCs, while γδ T/NK cells detect TFC dysregulation and recruit immune effectors—as an important mechanism in GD pathogenesis. This evidence concerns the gene ANXA2 and infection.