Moreover, in a mouse model of elevated IOP and in human eyes with primary open-angle glaucoma (POAG), the SIX6 risk variant (rs33912345, His141Asn) has been implicated in POAG pathogenesis through the upregulation of p16INK4a expression, which accelerates retinal ganglion cell senescence in the adult retina [75]. This evidence concerns the gene SIX6 and open-angle glaucoma.