Although the expression of ENaCβ, ROMK and Maxi-K in mouse GS model has been reported to be significantly increased in both immunoblotting and immunofluorescence of mouse kidney (6), the adaptive response of upstream and downstream Na+ and K+ associated transporters in response to renal Na+ and K+ wasting in GS patients remains unknown. The gene discussed is KCNJ1; the disease is Gerstmann syndrome.