Extranuclear or nongenomic effects of thyroid hormones are widely recognized, suggesting the existence of mechanisms independent of nuclear receptors and protein synthesis, involving plasma membrane, mitochondria, or cytoskeleton. Recently the plasma membrane receptor for thyroid hormone has been identified with the aVb3 integrin and this has widened the possible role of nongenomic effects of these hormones significantly. In particular thyroid hormones produce short-term effects on several important Na-dependent transport systems, the Na/H exchanger, amino acid transport System A, and the Na/K-ATPase, leading to a mitogenic response in embryo cells, whereas modulation of the same transport systems may have a different role in other cells such as the L-6 myoblasts in culture, where the activation of the Na/H exchanger may help the recovery from acidosis after muscle contraction. Recent results from the literature and from our laboratory show that thyroid hormones are able to modulate the activity of growth factors. They also show a nongenomic protective role toward oxidative stress for the immune system cells. It appears that thyroid hormones in many cases can modulate nongenomically the same targets which are affected by the nuclear receptors through long term mechanisms. These hormones also play a different role according to the cellular context, confirming an old theory that they help to keep the steady state level of functioning.