Analogous to lipopolysaccharide (LPS)-mediated downregulation of sterol synthesis in case of viral infections, limiting cholesterol biosynthesis in human macrophages and fibroblasts via genetic knockdown of sterol regulatory element-binding proteins [sterol-regulatory element-binding proteins (SREBPs), discussed in a later section], was reported to spontaneously engage type I IFN signaling and restrict infection (30–33). Here, CNBP is linked to infection.