Enormous scientific progress in molecular tumor biology and immune surveillance has resulted in the introduction of effective targeted therapies [e.g., by blocking the hyperactive B-rapidly accelerated fibrosarcoma (BRAF)‐mitogen-activated protein kinase (MEK) pathway that represents a hallmark of melanoma] and immunotherapies [including single or dual blockade of cytotoxic T lymphocyte-associated protein-4 (CTLA‐4) and programmed cell death protein-1 (PD-1)] for metastasized melanoma (1–4). The gene discussed is BRAF; the disease is neoplasm.