Non genomic effects of Thyroid Hormones (THs) do not require interaction with nuclear receptors, but are mediated by plasma membrane receptors, as a_Vb₃ integrin and by cytoplasmic isoform of TRb1, which can associate with PI3K-regulatory subunit p85a. Many of these effects can be mimicked by T₃-agarose, that cannot enter inside cell. In cultured chick embryo hepatocytes, T₃ mitogenic effect is dependent on short-term activation of PKC and MAPK, but it is not mediated by a_Vb₃ integrin, because neither T₃-agarose stimulates proliferation, nor RGD (inhibitory peptide of integrin) and tetrac (THs antagonist on integrin) block the mitogenic effect of T₃. Here we analyse if, at 14 and 19 days of prenatal life, T₃ non genomic effects on proliferation can utilise a signalling pathway involving PI3K/Akt, NOXs and ROS production. Hence, we have assayed: 1) effect of Wortmannin, LY294002, Diphenyleneiodonium (DPI) and ^®Pefabloc on T₃ stimulation of DNA synthesis 2) production of ROS, after T₃ treatment 3) effect of Wortmannin, LY294002, DPI and ^®Pefabloc on ROS production by T₃ 4) activation of PI3K/Akt pathway by T₃. Our data show that T₃ induces a moderate increase of ROS production, that Wortmannin, LY294002, DPI and^®Pefabloc, block the augment of DNA synthesis and of ROS production; moreover, we prove that T₃ is able to rapidly activate PI3K/Akt pathway. These results suggest a new way for T₃ non genomic effects, which involves NOXs activation by PI3K/Akt and production of ROS.