Accordingly, we predict that if we take advantage of our mouse model to direct expression of Erk1R84H to other tissues (i.e., skin, intestine, pancreas), tumors will be developed in those organs.The observation that Erk promotes cancer, while suppressing its own activity and probably activity of other pathway’s upstream components, may argue that when Erk1 is constitutively active, even at low level, RTKs and Ras effectors are not required for tumor maintenance. This evidence concerns the gene MAPK3 and neoplasm.