Although studies have reported that serotonin activates downstream targets of PI3K-AKt-mTOR and Jak1-STAT3-ERK1/2 to promote glycolysis and growth in breast [29], liver [30], and pancreatic ductal adenocarcinoma [31] tumors, the role of serotonin-induced immune response in the lesion site (tumor micro-environment) is largely unexplored. This evidence concerns the gene AKT1 and pancreatic ductal adenocarcinoma.