It has been suggested that activation of NCC in these models could be secondary (Ostrosky‐Frid et al, 2019); that is, given that recent studies suggest a role for KS‐WNK1 in the response to hypokalemia (Boyd‐Shiwarski et al, 2018), it is possible that KS‐WNK1 knockout mice have a potassium losing phenotype that could be compensated by a WNK4‐induced activation of NCC. The gene discussed is SLC12A3; the disease is Hypokalemia.