Most intercellular communication with high strength during infection occurred from fibroblast to epithelial cells via pathways involved in cell-cell adhesion/proliferation (Nectin, Cdh, Jaml), extracellular matrix remodeling (Collagen, laminin), growth factor action (Egf, Vrgf, Epgn), or immunomodulation (Cxcl, Mif, Sema4) (Fig. 3A). This evidence concerns the gene NECTIN1 and infection.