Our study elaborated a previously unrecognized role of the CCL3-CCR4 axis in the occurrence and development of NEC, which represents an important conceptual advance that CCL3 may be one of the key culprits of intestinal tissue damage in patients with NEC, and blocking CCL3, CCR4, or NF-κB may represent a novel effective immunotherapy for NEC. The gene discussed is NFKB1; the disease is necrotizing enterocolitis.