The IFNGR1 gene promoter construct that contained the -56 T allele showed higher transcriptional activity in LECs than did the construct with the -56 C allele after stimulation with IFN-γ, and there was higher IFNGR1 expression in the LECs in atopic than in senile cataracts [7], indicating that the -56 T allele in the IFNGR1 promoter leads to elevated IFNGR1 transcriptional activity and represents a genetic risk factor for atopic cataracts. Here, IFNGR1 is linked to senile cataract.