SLC12A3 and Hypokalemia: This assumption is supported by: (a) it has been suggested that most of alterations in SLC12A3 gene are inactivating mutations that impair gene transcription or translation in patients with T2DM and GS [33, 34], (b) This mutational damage would lead to a truncated/alterated NCC cotransporter polypeptide with a loss function causing impaired reabsorption of sodium chloride, potassium and magnesium in the DCT (see Fig. 2) [38, 39], (c) both hypokalaemia as well as hypomagnaesemia have been related to cause insulin secretion abnormalities [33, 40].