Duan et al. [76] found that immunoblotting and qPCR analysis in abnormally invasive placentas (AIP), including PA, PI, or PP, showed that CCN3 overexpression is accompanied by high levels of p53, p16, p21, cyclin D1, Notch-1 cleaved, pFAK, pAkt, and pmTOR, as well as low levels of pRb, suggesting that CCN3 mediates senescence by cell cycle arrest through the activation of the FAK-Akt-mTOR pathway and cleaved Notch-1/p21, contributing to increasing the invasion properties of EVT. Here, CCN3 is linked to autoimmune pancreatitis.