This intervention reduces Müller cell apoptosis and mitigates gliosis mediated by Glial Fibrillary Acidic Protein (GFAP) overexpression, potentially helping to maintain the supportive function of Müller cells for the BRB and mitigate structural damage to the BRB in diabetic retinopathy (98). The gene discussed is GFAP; the disease is diabetic retinopathy.