In addition to this “classical” aldosterone-induced K+ loss, another aspect likely contributes to the hypokalemia in EAST/SeSAME syndrome: Sorensen and colleagues found that NaCl reabsorption by the thiazide-sensitive NaCl transporter (NCC) is completely put at the service of K+ excretion under certain circumstances: in hyperkalemia, the increased K+ concentration is sensed by DCT cells and leads to inhibition of NCC (Sorensen et al., 2013). This evidence concerns the gene SLC12A3 and EAST syndrome.