The explanations for this difference (higher 131I cumulative dose administered in DTC/+T2DM patients than in those with DTC/−T2DM) converge towards NIS from two directions: (i) the presence of T2DM: there is the possibility that 131I uptake may be sufficiently high in the pancreatic tissues (especially in the islets of Langerhans), which are known to exhibit dysfunction in T2DM patients, to reduce 131I uptake in the remnant thyroid tissue [32]; and (ii) metformin treatment: metformin activates AMPK, leading to decreased NIS and thyroid 131I uptake. This evidence concerns the gene SLC5A5 and type 2 diabetes mellitus.