We found that neither PPARδ overexpression (Supplementary Fig. 4d, e) nor PPARδ activation by GW treatment (Supplementary Fig. 4f, g) increased p-ERK1/2 (Supplementary Fig. 4d, e, h, i) in the tested mouse and human PDAC cell lines, indicating that this in vivo PPARδ hyperactivation upregulated Il6/p-Stat3 and amplified KRASmu activity via indirect mechanisms, likely through remodeling the pancreatic tumor microenvironment (TME), rather than direct autochthonous effects. This evidence concerns the gene STAT3 and pancreatic neoplasm.