When lytic cycle is needed for the spreading of the virus, TGF-β disrupts the latency by stimulating the expression of BZLF1/Zta via both Smad-dependent and Smad-independent pathways which in turn, promotes the production of TGF-β and inhibits the transcription of EBNA1. Intriguingly, it has been shown that the EBV infection rate of epithelial cells can be enhanced by exogenous TGF-β1 and TGF-β1 derived from the epithelial cells facilitated viral transmission by inducing lytic cycle in the donor B-cells in co-culture systems [171,172]. Here, TGFB1 is linked to Epstein-Barr virus infection.