While compelling evidence establishes ferroptosis as a key driver of cyst progression in ADPKD—linked to PKD1/PKD2 mutations, disrupted antioxidant networks (GPX4/SLC7A11), iron overload, and lipid peroxidation—and validates ferroptosis modulators as potential therapeutics, several critical, insufficiently addressed research gaps persist. Here, GPX4 is linked to autosomal dominant polycystic kidney disease.