On the one hand, the degradation of CD2AP TGF-b1 secretion is also promoted, which can inactivate the anti-regulatory signal TGF-b1-CD2AP-PI3K-ATK and enhance the pro-apoptotic signal TGF-b1-Smad3-P38 [140], but interestingly, PI3K-ATK is in an inhibited state only in the middle stage of PRRSV infection [141], which may be the result of the virus in the middle stage of infection in order to breaking the barrier effect of alveolar epithelial cells for invasion of the organism and cell-to-cell spreading. Here, TGFB1 is linked to infection.