It could be speculated that in cancer constitutive activation of MAP kinase could be triggered by upstream oncogenic regulators due to the presence of paracrine/autocrine growth factor stimulation, rather than Ras or B-raf mutations or components of the various other signal transduction pathways that interact with MAPK, since the mutation of K-ras and B-raf obviously constitutes one of multiple ways to activate this pathway. This evidence concerns the gene BRAF and cancer.