In such situations, ERK is part of the signaling cascade while the constitutive activation may either stem from an activating, oncogenic mutation of a key receptor such as Epidermal Growth Factor Receptor (EGFR, usually treated by Gefitinib [19]) or by a kinase mutation (most well known are B-Raf and Ras mutations, however, in some aggressive cancers this can also be ERK mutations). This evidence concerns the gene BRAF and cancer.