This nicely fits into a model, in which flow sensing in the ADPKD background is disturbed, leading to a dysregulation of second messenger dynamics: due to mutations in PC1/PC2, the Ca2+ homeostasis is disturbed and Ca2+ influx reduced, which would result in chronic activation of the ciliary localized, Ca2+‐inhibited AC5 and AC6 and, in turn, an increase in ciliary cAMP levels (Choi et al, 2011; Sussman et al, 2020). Here, ADCY5 is linked to autosomal dominant polycystic kidney disease.