NR1H4 and pancreatic neoplasm: 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).