The tear film has a heterogeneous structure. Next to the ocular surface is a region hundreds of nanometers thick that is rich in mucin polymers. Atop this so-called mucus layer lies the aqueous layer, which is up to 5 microns thick. The outer surface of the aqueous layer is covered by a thin lipid layer that is exposed to the ambient air. The mucin protects the ocular epithelium against pathogens, and clinical evidence points to progressive destruction of the membrane-associated mucins (MAM) in eye infection. From a fluid mechanical viewpoint, the MAM modifies the wetting condition on the solid substrate, and modulates the van der Waals forces between the interfaces. We hypothesize that a change in the configuration of the MAM, say from complete coverage to partial coverage, induces a stronger van der Waals attraction and enhances slip on the ocular surface. Both factors should accelerate the breakup of the tear film. This will explain clinical observations of faster tear-film breakup in various eye diseases. We numerically simulate the tear-film breakup process to study the effect of the MAM through an elevated Hamaker constant and a modified slip length. Results show that the loss of MAM indeed precipitates tear-film breakup, and suggest that the tear-film breakup time can be a potential diagnostic of eye diseases.