In 2010, a humanized mouse model for studying neonatal hyperbilirubinemia was developed [48], where the authors showed that breast milk feeding suppressed the intestinal expression of UGT1A1 through the IkB kinase/nuclear factor-kB(IKK/NF-kB) pathway, whereas liver UGT1A1 expression was still minimal, the combination of which led to the development of BMJ [49]. The gene discussed is NFKB1; the disease is Hyperbilirubinemia.