On the contrary, we showed an impaired TRPV4‐dependent Ca2+ influx and deficient channel glycosylation in freshly isolated monolayers of cystic cells of PCK453 rats, a homologous model of human ARPKD (Zaika et al., 2013), and in primary cultured cystic cells of human ADPKD kidneys (Tomilin et al., 2018) pointing to a common underlying mechanism associated with channel dysfunction in driving cystogenesis. Here, TRPV4 is linked to autosomal dominant polycystic kidney disease.