Constitutively active Ras mutants that do not exchange bound GTP have been identified in about 30% of all tumors, although they are more prevalent in some tumor types than in others Persistent activation of ERK by mutated Ras or Raf proteins contributes to tumor cell proliferation; indeed the transforming potential of Ras or Raf mutants is absolutely dependent on the downstream MEK and ERK proteins, thus providing an impetus for development of inhibitors of MEK or ERK (Kohno and Pouyssegur, 2003) as therapeutic agents. This evidence concerns the gene MAP2K7 and neoplasm.