When the premature intestine with accompanying elevated expression levels of TLR4 becomes colonized, in the setting of the correct environment that favors exaggerated TLR4 signaling, TLR4-mediated enterocyte apoptosis and delayed mucosal repair ensue, which together favor bacterial translocation and the development of systemic sepsis and NEC (see Figure 1). The gene discussed is TLR4; the disease is necrotizing enterocolitis.