Scientists have indicated that overexpression of MUC1 in pancreatic and breast cancer cells can elevate synthesis and secretion of tumor angiogenic response, particularly VEGFs, via activation of intracellular signaling pathways such as Ras/mitogen-activated protein kinase (MAPK), Jak/Stat, and phosphoinositide 3-kinase (PI3K)/AKT/mechanistic target of rapamycin (PI3K/AKT/mTOR) [39, 40]. This evidence concerns the gene MUC1 and neoplasm.