On the other hand, CD133+ population, which represents immature progenitor cells, was reduced in correlation with higher AGE levels, suggesting that the accumulation of AGE in OSA subjects whose condition remain untreated for a long time could jeopardize the EPC pool and may forebode impairment of vascular repair capacity and endothelial dysfunction. This evidence concerns the gene PROM1 and obstructive sleep apnea syndrome.