It is plausible that many—and perhaps most—growing cyst cells in human ADPKD are not null for PC1 and that overexpression of PC1-p30 and/or PC1-p15 occurs as a response to oxidative stress and promote the observed Warburg-like metabolic changes that lock these cells into a glucose-dependent, metabolically inflexible state. This evidence concerns the gene PKD1 and autosomal dominant polycystic kidney disease.