A previous study has also demonstrated that yeast-derived β-glucan could reduce intestinal injury in rat model of NEC by affecting intestinal expression of IL-18, TNF-α, iNOS, CXCL1, Tff3, and Muc-2, which suggests that β-glucan might possess potential in the treatment of NEC via reduction of inflammatory response within the intestine [33]. The gene discussed is CXCL1; the disease is necrotizing enterocolitis.