Examples include: HER2 amplification in breast cancer which is responsive to trastuzumab [8,9]; BRAF mutation in melanoma which predicts responsiveness to BRAF/MEK inhibitor therapy [10,11,12]; KRAS wild-type tumours in colorectal cancer which are sensitive to anti-epidermal growth factor receptor (EGFR) therapies [13,14] and EGFR mutations and ALK gene rearrangements in non-small-cell lung cancer, which are sensitive to EGFR and ALK inhibitors, respectively [15,16]. The gene discussed is BRAF; the disease is neoplasm.