This is expected because, as mentioned above, the nursing infants in Group I manifested predominantly respiratory infections and pneumonia, and CXCL10, as well as the CXCR3 receptor, is highly induced by IFN-γ and type I IFN via NF-κB activation during infection, injury, or inflammatory responses, such as multiple sclerosis, skin and mucous membrane inflammation and bronchiolitis (28–34). This evidence concerns the gene NFKB1 and pneumonia.