AKT1 and pancreatic neoplasm: Treatment of human pancreatic cancer cells (MIA‐PaCa‐2) and human in situ pancreatic adenocarcinoma cells (BXPC‐3 cells) with different β‐sitosterol concentrations (0, 125, 250, and 500 μM) inhibited cancer cell migration and invasion by regulating EMT pathway key molecules (dose‐dependently down‐regulating Snail and vimentin proteins and up‐regulating E‐cadherin protein), thereby exerting anti‐pancreatic cancer activity by inactivating the AKT/GSK‐3 signaling pathway and regulating apoptosis.135