This bioinformatic analysis was further validated using western blotting assay in Capan1 transfected with a vector or different doses of FLAG-tagged N1DARP plasmid, where overexpressed N1DARP suppressed the activation of Notch, Hedgehog, JAK-STAT3, and PI3K-AKT pathways in a dose-dependent manner (Fig. 4b), which are well-established signaling pathways related to tumor initiation and progression of pancreatic cancer. The gene discussed is STAT3; the disease is neoplasm.