Moreover, increased IFN-γ expression has been observed in Hif-1α-deficient CD4+ T cells cultured under high-glucose conditions, accelerating DKD progression, suggesting that targeting the high glucose/Hif-1α transcription axis may help prevent DKD by limiting IFN-γ secretion from Th1 cells (223). The gene discussed is CD4; the disease is diabetic kidney disease.