A previous study using a mouse model of pancreatic neuroendocrine tumorigenesis (PNET) suggested that interstitial fluid pressure led to invasion progression by activating NMDAR and its downstream MEK-MAPK and Ca2+/calmodulin-dependent kinases (CaMK) effectors, ultimately caused the activation of CREB [20]. Here, MAP2K7 is linked to primitive neuroectodermal tumor.