EMAP-II decreases the viability of pancreatic ductal adenocarcinoma cells through inhibition of fibronectin-dependent proliferation (Schwarz et al., 2010); low-dose (0.05 nM) EMAP-II also induces the apoptosis of C6 glioma cells via the mitochondrial pathway (Liu et al., 2015b). Here, FN1 is linked to pancreatic ductal adenocarcinoma.