Autoimmune thyroid disease (AITD), including Graves' disease (GD) and Hashimoto's thyroiditis (HT), affects around 5% of the overall population, making it one of the most common autoimmune disorders. In the age of precision medicine, treatments can be customized to an individual's genetic makeup and environmental background, providing three main advantages: symptoms relief, prevention of diseases, and even reversal of diseases. Currently, the available treatments for thyroid autoimmune disorders are not designed to target the autoimmune process and merely offer relief from symptoms. Introducing targeted treatments in the management of AITD requires a thorough comprehension of the key drivers of the disease. Certain genes have been found that make individuals more susceptible to develop AITD, such as the thyroid-specific Tg and TSHR genes, as well as the immunoregulatory HLA-DR3 and CD40 genes. Interestingly, SNP variations and epigenetic alterations might initiate AITD by triggering a range of immunological issues, such as abnormal presentation of self-antigens during the acquisition of immune tolerance, defective binding of self-peptides to MHC, and aberrant stimulation of B and T cells. Blocking any of these autoimmune-causing mechanisms is a novel approach to prevent the development of overt clinical illness. New advances over the last few years have provided evidence on the role of the microbiota, mi-RNA and DNA methylation in the pathogenesis of GD and/or its extrathyroidal manifestation, particularly Graves’Orbitopathy (GO).

Overall, the recent findings related to epigenetics provide a framework for identifying novel treatment targets.

The primary goal of this special issue is to discuss novel acquisition in AITD pathogenesis, with particular interest to the epigenetic novelties that could be used as new tools in the diagnosis and the development of novel drugs for patients with AITD, with particular interest in GD and GO. Original research articles, reviews, and case studies to overview the most recent basic and clinical researches will be included.

Potential topics include, but are not limited to:

• New insight into AITD pathogenesis
• New diagnostic tools and therapeutic option for GD and GO
• New acquisitions in thyroid autoimmunity, with a special focus on epigenetics