Thus, it has been demonstrated that PPARγ inhibition facilitates FTC onset through NF-κB-dependent cyclin D1 activation and critical apoptotic genes repression [46], and that PTEN deficiency boosted thyroid cancer progression as a consequence of NF-κB-mediated tumor cell survival enhanced by AKT activation [47]. The gene discussed is AKT1; the disease is thyroid gland carcinoma.