NFKB1 and thyroid cancer, nonmedullary, 2: 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].