Our main findings in this model include: 1) the disappearance of the high ouabain affinity that a subpopulation of NKA has in ADPKD; 2) the significant reduction in kidney cystic area and fibrosis to the basal levels of the Pkd1RC/RC mouse model; 3) the decrease in ouabain-dependent cell proliferation that is a main driver of ADPKD cystogenesis [27]; and 4) lack of activation of ERK and Akt, two key mediators of NKA signaling induced by ouabain [21,27]. Here, AKT1 is linked to fibrosis.