Although all 4 mutants present certain degree of loss of NKA function,14,15 only 3 variants appear to carry passive inward “leak” currents similar to those observed in most ATP1A1 somatic variants from aldosterone-producing adrenal adenomas, which cause hyperaldosteronism and secondary hypertension.16,29,30 Many ATP1A231 and ATP1A332,33 variants have also been reported to carry inward currents. The gene discussed is TAC1; the disease is secondary hypertension.