Because high glucose is able to increase expression of HIF-1α in the glomeruli of animal models of diabetes in conditions of normoxia [16], it is plausible that patients harboring the T/A+A/A genotypes do not present an increase in p22phox transcription rate as high as that observed in patients harboring the T/T genotype in response to HIF-α, which could result in lower ROS generation in conditions of hyperglycemia. The gene discussed is HIF1A; the disease is Hyperglycemia.