A recent study by Niño et al. (2018) demonstrated a gut-brain signaling axis in a mouse model of NEC in which activation of intestinal TLR-4 signaling led to release of high-mobility group box 1 (HMGB1) protein in the intestine, which in turn, promoted activation of TLR-4 on brain microglial cells resulting in accumulation of reactive oxygen species, loss of oligodendrocyte premature cells, dysmyelination, and cognitive impairment. The gene discussed is TLR4; the disease is Cognitive impairment.