[1][2] Features of this syndrome include Peters' anomaly, corneal opacity, central defect of Descemet's membrane, and shallow anterior chamber with synechiae between the iris and cornea.

[citation needed] Craniofacial abnormalities commonly seen in patients with PPS include hypertelorism, ear malformations, micrognathia, round face and broad neck, and cleft lip and palate.

[4] The beta 3-glucosyltransferase enzyme is responsible for glycosylation, the attachment of sugars to proteins, which through this modification allows for performance of a wider variety of functions.

[6] A study of 55 patients with Peters-plus-related phenotypes, but lacking the most common combination (Peters anomaly, short stature, and brachydactyly), revealed none of those cases displayed mutation in the B3GLCT gene.

Thus PPS-like signs and symptoms, when they occur independently of each other, provide strong evidence that the B3GLCT gene mutation is in fact responsible for actual cases Peters-plus syndrome.