AKT1 and pancreatic neoplasm: Pancreatic cancer cell-derived exosomes inhibited glucose intake and promoted lipid deposition, causing skeletal muscle atrophy by inducing insulin resistance [27], which was partly controlled by the PI3K/Akt/FoxO1 signaling pathway, and exosomal miRNAs such as miR-125b-5p, miR-540-3p, miR-450b-3p, and miR-666-3p may potentially contribute to pancreatic cancer-induced cachexia [17].