Furthermore, the expression of LGALS3BP is upregulated in both chronic and acute viral infections, perhaps due to its induction by a variety of molecules that “either mimic or are characteristic for an ongoing inflammation and microbial infection, such as IFN-α, IFN-β, IFN-γ, TNF-α, poly(I:C), dsRNA, and dsDNA”, as thoroughly reviewed by Loimaranta et al. [45]. This evidence concerns the gene IFNB1 and viral infectious disease.