KRAS and pancreatic neoplasm: Third, basic research reports that have used pancreatic cancer cells wherein KRAS function had been inhibited by CRISPR/Cas show that these cells not only activate phosphoinositide 3‐kinase (PI3K)‐dependent mitogen‐activated protein kinase signaling, but also induce metastasis‐related cascade, including EMT (TGFB2, PBX1, and FGFBP1), cell adhesion (FLRT3 and ICAM1), and extracellular matrix breakdown (MMP19 and MMP28).27