In summary, we suggest that: 1) VTCN1 is a critical regulator of TB syncytialization, TB invasiveness and possibly other aspects of differentiation in the early human placenta; 2) VTCN1 limits upregulation of classical MHC Class I genes and an array of proteins involved in interferon responses in TB, including that of IFITM1, a protein whose expressions counteracts syncytialization; and 3) VTCN1 presentation by TB cells can induce phenotypic changes in peripheral natural killer cells that resemble those characteristics of the maternal-fetal interface. This evidence concerns the gene VTCN1 and tuberculosis.