Eliminating this motif (Pkd1Δ17) improves mRNA stability, raises Polycystin-1 levels, and alleviates cyst growth in cellular, ex vivo, and mouse PKD models.[37] Similarly, Pkd2 is inhibited via its 3′-UTR miR-17 motif, and Pkd2Δ17-induced Polycystin-2 derepression retards cyst growth in Pkd1-mutant models.[37] These findings suggest that evading 3′-UTR cis-interference and enhancing PKD1/2 mRNA translation is a potentially mutation-agnostic approach to arresting ADPKD. The gene discussed is PKD2; the disease is cyst.