In this study, we showed that NR5A2 promoted pancreatic cancer progression by inducing GDF15 expression, suggesting that the pro-tumorigenic roles of NR5A2 and BRD4 in pancreatic cancer could be reversed by GDF15 inhibition, making GDF15 a promising therapeutic target (Fig. 8G). This evidence concerns the gene GDF15 and familial pancreatic carcinoma.