A potential candidate is ENAC given that its loss of function causes hyperkalemia and metabolic acidosis [54], which would explain why tBS patients have normal potassium and bicarbonate values, but not a profound hypokalemic metabolic alkalosis, which would result from dual inhibition of NKCC2 and NCC alone (as seen, patients subjected to sequential nephron blockade by administering furosemide and thiazide to block NKCC2 and NCC, respectively [55]). The gene discussed is SLC12A3; the disease is Hyperkalemia.