Low mutation burden in recurrent glioblastoma patients was recently associated with longer survival after immunotherapy, implicating that tumor mutational burden itself may not be a causative driver of response to immunotherapy, but may reflect the immunological status of tumor or some other co-related feature, among them time to recurrence, TP53 mutation and any differences in the clinical care between patients with high vs. low mutational burden [108]. The gene discussed is TP53; the disease is glioblastoma.