ERK1/2 were constitutively activated without the external stimuli in both tumor cell lines, and this phosphorylation of ERK1/2 was diminished by the treatment of U0126 (Figure 4A), a potent and specific inhibitor of MEK1/2, which binds to MEK1 and MEK2 regardless of its activation state to inhibit ERK1/2 phosphorylation noncompetitively. This evidence concerns the gene MAP2K1 and neoplasm.