In pancreatic ductal adenocarcinoma (PDAC), elevated COX-2 expression promotes angiogenesis through EGFR/p38-MAPK/specificity protein-1 (Sp1)-dependent signaling [267], and inhibition of COX-2 leads to decreased angiogenesis and tumor growth in a VEGF-dependent manner [267,268]. This evidence concerns the gene SP1 and pancreatic ductal adenocarcinoma.