Diabetes leads to dysfunction of Müller cells and they assume a reactive phenotype, characterised by upregulation of glial fibrillary acidic protein (GFAP), inflammatory cytokines [IL-1β, IL-6, IL-8 and TNFα (encoded by Il1b, Il6, Cxcl15 and Tnf, respectively)] and neurotrophins (BDNF, CNTF, GDNF, NGF and NTF3), and downregulation of glutamine synthetase (GS, encoded by Glul), to mitigate tissue damage prior to clinical manifestations of DR (Reichenbach and Bringmann, 2010; Takeuchi et al., 2015; Boss et al., 2017; McDowell et al., 2018). Here, GLUL is linked to diabetes mellitus.