In human pancreatic ductal adenocarcinoma tissues, the tumor tissues express lower levels of PRKD1 than non-tumor tissues; PRKD1 usually acts by inhibiting cell motility and its loss/reduction, which reduces the phosphorylation of cortactin (substrate for PRKD1), thus causing an increase in F-actin l at the plasma membrane, is associated with a strong increase in sEVs secretion. This evidence concerns the gene PRKD1 and pancreatic ductal adenocarcinoma.