Other studies have shown that excess I promotes FTC apoptosis by activating the hypoxia-inducible factor 1alpha (HIF-1α)-mediated hypoxia signaling pathway and increasing N-myc downstream regulated 1 (NDRG1) expression and inhibits FTC proliferation in a dose-dependent manner [145]. Here, HIF1A is linked to thyroid cancer, nonmedullary, 2.