BST2, serving as a functional ligand for the ILT7 receptor, modulates tumor immune responses through a dual mechanism: firstly, by binding to the ILT7 receptor, it inhibits the secretion of type I interferon (IFN) mediated by TLR9/TLR7 in plasmacytoid dendritic cells (pDCs), thereby weakening their antiviral and antitumor activity; secondly, it synergistically enhances the inhibition of pDC activation through interaction with the transmembrane adhesion receptor CD44 [34]. This evidence concerns the gene IFNA1 and neoplasm.