OVOL2 and posterior polymorphous corneal dystrophy: In support of this proposed mechanism, a transcriptomic profile of PPCD corneal endothelial cells derived from a subject with PPCD3 harboring a pathogenic ZEB1 mutation and a PPCD-affected individual with unknown molecular cause, with no potentially pathogenic variant detected in ZEB1 or the OVOL2 promoter using the methods employed, revealed a significant decrease in ZEB1 expression compared to controls.21