Neuroinflammation is an important mechanism underlying the pathogenesis of traumatic brain injury [37, 38], while microglia are potent immune effector cells producing and releasing proinflammatory and cytotoxic mediators in response to brain injury [23] Therefore, the GPR110-dependent microglial production of cAMP (Fig. 2), a well-established regulator of immune responses [39], is likely an important contributing mechanism to the effectiveness of GPR110 ligands on rCHIMERA-induced optic tract gliosis (Figs. 4 and 5, S1-S2) and visual dysfunction observed in this study (Fig. 7, S3). This evidence concerns the gene ADGRF1 and brain injury.