Recent advances in thyroid research are reviewed which reflect fundamental changes in understanding of the pathogenesis of thyroid adenomas, and of clonal and polyclonal goiter nodules. It is generally accepted that chronic iodine deficiency leads to the development of a diffuse homogeneous goiter. However, low iodine supply does not explain generation and growth of thyroid nodules and the characteristic functional heterogeneity of most nodular goiters. Molecular analyses of recent years have revealed that thyroid adenomas and most nodules in goiters, even if morphologically heterogeneous, are clonal and thus true benign tumors. This has been demonstrated in areas both with iodine deficiency and with sufficient iodine supply. However, in areas with iodine deficiency, chronic stimulation accelerates the genesis of nodules and adenomas. The molecular pathogenesis of these tumors is still unknown. Only in a subgroup of toxic adenomas mutations of the TSH receptor and the Gs-alpha gene have recently been found that may explain the genesis of these tumors and the development of hyperthyroidism in patients with these adenomas.