While the RET/PTC1 rearrangement can stimulate the MAPK pathway in thyroid cancer cells [10], the transduction of either NRAS Q61R or BRAF V600E into TPC1 cells induced a strong, ~three-fold increase in the endogenous level of ERK1/2 phosphorylation (Figure 6A), consistent with a robust upregulation of MAPK pathway activation and MEK activity in these cells. This evidence concerns the gene BRAF and thyroid gland carcinoma.