We currently face a growing body of evidence showing that BRAF inhibition (with and without concurrent MEK inhibition) may trigger the development of cancer from pre-neoplastic lesions (e.g., melanoma and non-melanoma skin cancer, pancreatic cancer) or drive progression of existing but unrecognized cancers (e.g., colon cancer) (5–12). The gene discussed is BRAF; the disease is skin cancer.