Our group pioneered several years ago, in creating the first Alport syndrome mouse model which inherits a glycine substitution mutation in the COL4A3 gene, in contrast to several previous models that were knock-out models, that is one of the collagen IV genes was totally inactive. Our model recapitulates the clinical and morphological features of about 50% of all patients who carry similar mutations. The mutation we chose to introduce to this mouse model is the one most prevalent amongst all Cypriot patients with thin basement membrane nephropathy, a condition which fall under the Alport syndrome spectrum disorders, known as COL4A3:p.Gly1334Glu. The project has progressed to the point that based on important findings regarding the molecular and cellular basis of the disease, we administer synthetic repurposed chaperones for treating these mice, with promising results. A repurposed drug is one which has approval for another disease but is found to also have a positive impact on another medical condition.