Although the exact biological mechanisms have not been identified, TD may share genetic vulnerabilities with allergic disorders, which may include the dysregulation of excitability in cortical-basal ganglia (CBG) loops mediated by gamma-aminobutyric acid (GABA) transmission, a mediating role of cell adhesion molecules (CAMs) in hyperinflammation, and initiation of cytokines such as tumor necrosis factor and interleukins [39, 74–76]. Here, TNF is linked to thanatophoric dysplasia.