Introduction: Thyroid ophthalmopathy (TAO) is a rare autoimmune disorder in euthyroid patients; less frequent in those with negative autoantibodies and thyroid cancer. TSH-R stimulating antibodies bind to said receptor in orbital fibroblasts, producing the secretion of cytokines, hyaluronic acid and adipogenesis that contribute to TAO1. Clinical case: 54-year-old woman has had orbital alterations compatible with TAO for four years, CAS score 2/7-Eugogo Mild, studies of thyroid function and TSI/AbTPO/AbTg antibodies in normal ranges; therefore, she received oral corticotherapy and subtenonial corticosteroid injections. She was subsequently evaluated in Endocrinology, where goiter was found. Thyroid ultrasound showed hypoechogenic left thyroid nodule (14 mm), FNA: Bethesda VI and Pathological anatomy: Papillary thyroid carcinoma. She received ablative therapy with I-131 (30 mCi). Currently with excellent response. During follow-up, ophthalmologic evaluation showed: CAS score 0/10 and VISA score 0/10. Presents palpebral retraction, corneal erosions and PIO elevation. In Tomography: increase in volume of the lacrimal glands and extraocular muscles predominantly in the upper and medial rectum, as well as a thickening of the upper eyelid lift muscle, with greater involvement in the left orbit. These findings are compatible with inactive TAO with an expansive “white eye” phenotype, generally with a lower risk of compressive neuropathy.Discussion: In addition to normal thyroid function and mild TAO, the patient has the characteristic of presenting negative antibodies. Associated with TSH-R, factors such as IGF-1 can be found in the pathogenesis of TAO, which can generate a similar effect1. Likewise, IGF-1 stimulates cell proliferation, and is related to neoplasms such as thyroid carcinoma2. Conclusions Differentiated thyroid carcinoma should be ruled out in all patients with TAO, whether euthyroid or not. Studies confirming the relationship of IGF-1, TAO and thyroid carcinoma are necessary.