Many factors may contribute to the constitutive NF-κB activation in thyroid cancer: chronic extracellular stimulation of NF-κB signaling-related receptors, crosstalk with signal pathways strongly activated in thyroid carcinoma cells (MAPK, PI3K/AKT, RET/PTC, BRAF, RAS), or genetic alterations of one or more members of the NF-κB signaling cascade. The gene discussed is AKT1; the disease is thyroid gland carcinoma.