Interestingly, we did see that likely ROMK channel activity is increased in SPAK KO mice in the PCs, suggesting a likely compensated effect, also in the absence of the BK channel, which could explain why SPAK KO mice did not exhibit a hyperkalemia phenotype, rather than hypokalemia, one of the Gitelman syndrome phenotypes. The gene discussed is KCNMA1; the disease is Hypokalemia.