This is similar to the concept that Kir4.1/Kir5.1 serves as a potassium sensor in the DCT to regulate Na+ reabsorption through the sodium chloride cotransporter (Manis et al., 2020; Su et al., 2019) explaining hypokalemia observed in rodents and humans lacking functional Kir4.1/Kir5.1 channels (Celmina et al., 2019; Cuevas et al., 2017; Malik et al., 2018; Palygin, Levchenko, et al., 2017; Schlingmann et al., 2021; Su et al., 2019; Tomilin et al., 2018). This evidence concerns the gene KCNJ16 and Hypokalemia.