Moreover NE stimulates cell proliferation and other cancerous biological behaviors of pancreatic ductal adenocarcinoma (PDAC) cells via β-adrenergic receptor-dependent activation of p38 mitogen-activated protein kinases (p38/MAPK) pathway [15], and at the same time was able to inhibit apoptosis and promote cell survival of cancer cells, binding β2-ARs in a Notch-1-dependent manner [16]. This evidence concerns the gene MAPK14 and pancreatic ductal adenocarcinoma.