The effects of stably-expressing EYA2 in pancreatic cancer cells we observed on TGF beta pathway gene expression may be of particular interest since the TGF beta signaling pathway is disrupted in many pancreatic cancers and as evidenced by the inactivating mutations in DPC4 in ~55% of pancreatic cancers and the occasional genetic inactivation of other pathway components (TGFBR2, TGFBR1, BMPR2)[3, 5, 34, 35]. The gene discussed is SMAD4; the disease is pancreatic neoplasm.