This principle becomes more complex with tumor recurrence and treatment, and even genetic alterations thought to be foundational to tumorigenesis, such as IDH mutation, may become subclonal and relegated to “passenger mutation” status with tumor evolution, while other newly acquired mutations may emerge in dominant clones and drive tumor biology [17, 65, 100, 132, 138, 142, 215]. The gene discussed is IDH1; the disease is neoplasm.