The studies taken together highlight a few key findings of the pathophysiology of NEC: 1) intestinal inflammation and injury translates to neural changes that are proposed to occur through TLR4 signaling in the intestine, 2) endogenous ligands released from intestinal TLR4 activation go on to activate TLR4 on microglia and 3) downstream neurologic changes occur including microglial activation, increased neuroinflammation, and decreased myelination which can lead to downstream neurodevelopmental deficits. Here, TLR4 is linked to necrotizing enterocolitis.