82. Thus, CH5126766 inhibits the feedback induction of MEK phosphorylation that occurs after ERK inhibition in cancer cells exposed to other MEK inhibitors. Nagarajah et al. reported that CH5126766, an allosteric MEK inhibitor, suppressed ERK in a sustained manner by blocking RAF reactivation, whereas selumetinib, an MEK inhibitor, suppressed ERK activation transiently in a tumor harboring the BRAF mutation 83. Sustained ERK inhibition via CH5126766 treatment induced higher RAI uptake and 131I-mediated therapeutic effects (Table 1). This evidence concerns the gene MAP2K7 and cancer.