The dual role of HIF-1α in kidney disease is further supported by studies showing that tubular-specific deletion of HIF-1α in diabetic mice exacerbates mitochondrial dysfunction and ROS accumulation, leading to tubular damage [27], while HIF-1α deficiency accelerates pathological changes in the early stages of DKD, particularly affecting podocyte survival and glomerular injury [29]. The gene discussed is HIF1A; the disease is diabetic kidney disease.