have proposed that DDIT4 deficiency results in oncogenic transformation by augmenting ROS‐cleansing NADPH to skew cellular metabolism.[11] On the contrary, DDIT4 can also promote the pathogenesis of diabetic retinopathy by mediating ROS‐induced degradation of the antioxidant transcription factor NRF2.[12] Currently, there is insufficient evidence regarding the transcriptional regulation of DDIT4 during liver injury or its pathophysiological implication. Here, DDIT4 is linked to diabetic retinopathy.