This very fact in combined with our finding that FXR was positively correlated Sp1 and the discovery that phosphorylated Sp1 was the activated form of Sp1 promoted us to proposed a model to link FXR to Sp1: BAs-triggered FXR increase the over-activation of p38-MAPK and/or PI3K/AKT signaling in the plasma resulting in the phosphorylation of Sp1, which finally activate the expression of genes associating with the malignant phenotype of pancreatic cancer (Figure 4). This evidence concerns the gene AKT1 and pancreatic neoplasm.