Abnormal thyroid function may promote breast cancer through the action of thyroid hormones and their stimulation of αvβ3 integrin receptor inducing mitogen-activated protein kinase (MAPK) activity and the estrogen receptors pathway response; the interaction of TSH and TSH-stimulating antibodies in the course of Graves’ disease on the extra thyroid receptors for TSH (TSH-R) localized in breast tissue; and the action of an increased concentration of prolactin (PRL) accompanying the primary hypothyroidism. This evidence concerns the gene PRL and breast carcinoma.