Overexpression of the trimeric intracellular cation channel TRIC-B (potassium channel) corrects defects in ER calcium ion release and inhibits cyst formation, whereas TRIC-B deficiency exacerbates cyst formation in Pkd2 heterozygous kidneys, which suggests that PKD2 in the ER may function as a potassium ion channel, facilitating potassium–calcium ion exchange and thereby regulating intracellular calcium ion concentrations through IP3R-mediated mechanisms [72]. Here, KCNA3 is linked to cyst.