Understanding the physiological role of SP-A in modulating excessive inflammation in neonatal intestine and the molecular mechanism by which SP-A reduces TLR4 in epithelial cells can potentially lead to the use of SP-A as a biomarker for and prophylactic agent against the onset of excessive inflammation that can lead to intestinal diseases such as NEC in premature infants. This evidence concerns the gene TLR4 and necrotizing enterocolitis.