As NRF2/NFκB-pathways regulate the redox homeostasis, oxidative stress, and inflammatory response, an imbalance between NRF2 and NFκB pathways clearly prompt neurodegeneration, autoimmunity, and tumors, sustaining the neurodegenerating state, as observed in diabetic retinopathy and proliferative vitreoretinopathy associated with ERM development and formation, acting at both transcriptional/post-transcriptional levels inside a specific ERM environment, and reinforcing the neuroinflammatory response, as observed in diabetic retinopathy [43, 44]. This evidence concerns the gene NFE2L2 and Autoimmunity.