Consistent with this view, it has been proposed that FOXC1 haploinsufficiency (50% of the normal activity) underlies dominant glaucoma in ARA patients [35] and increased gene dosage due to heterozygous gene duplications (150% activity, representing the upper activity value of this model compatible with alterations limited to the eye), causes dominant inherited anterior-chamber defects associated with developmental glaucoma [49]. The gene discussed is FOXC1; the disease is glaucoma.