These findings have been reproduced in an external cohort and fall in line with a recent theory concerning the development of NEC; we observe a community with either high levels of LPS that could stimulate the TLR4 receptor leading to inflammation, or low CpG frequencies which could lead to reduced TLR9 signalling and reduced IRAK-M dependent inhibition of TLR4 [7]. This evidence concerns the gene IRAK3 and necrotizing enterocolitis.