Thyroid eye disease or thyroid-associated orbitopathy (TAO) is the commonest cause of orbital disease with an inflammatory component. With a basic knowledge of both orbital anatomy and the pathogenesis of TAO, it is easy to understand how its typical constellation of features originates. These features can be considered as primary or secondary. Primary features are those due directly to the disease process affecting a tissue e.g. restrictive myopathy. Secondary features occur due to the interaction of the affected tissue and the anatomical configuration of the tissues e.g. corneal ulceration or optic neuropathy, and are less likely to be florid at presentation. TAO is characterized by an immune-mediated inflammation of the orbital structures. Expression of the thyrotropin receptor on orbital pre-adipocytes leads to aberrant targeting of the anti-thyroid immune response to the orbit. Inflammatory cytokines are released attracting a lymphocytic infiltrate and causing glycosaminoglycan accumulation in the extraocular muscles, leading to inflammation and proptosis. More recently, recruitment of circulating fibrocytes, a form of mesenchymal progenitor cell, has been implicated. Several genetic variants have been proposed to have a role in TAO, such as MHC or CTLA4 molecules, although TAO rarely seems to run true even in families with several members who have hyperthyroid Graves’ disease. More likely, the accumulation of several genetic variants leads to a more severe autoimmune phenotype in TAO, and none of these variants has thus far been confirmed to be specific for TAO.