Graves’ disease is the main differential diagnosis of familial nonautoimmune hyperthyroidism. Two heterozygous activating germline mutations of the thyroid-stimulating hormone receptor (TSHR), associated with familial nonautoimmune hyperthyroidism, were first described in two families with autosomal dominant hyperthyroidism involving residues in the third and seventh transmembrane domains. Activating mutations of the TSHR have been described in familial nonautoimmune hyperthyroidism, sporadic congenital nonautoimmune hyperthyroidism, and autonomously functioning adenomas. Subclinical hyperthyroidism is more prevalent in patients with multinodular goiter and is a risk for cardiovascular morbidity and mortality. The aim of treatment of a patient with a multinodular goiter is the reduction of goiter size and the prevention of thyrotoxicosis. Subacute lymphocytic thyroiditis and postpartum thyroiditis are variants of chronic autoimmune thyroiditis. Synonyms are silent thyroiditis, hyperthyroiditis, atypical thyroiditis, and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism. The prevalence of subacute lymphocytic thyroiditis varies widely.