Based on their own previous work—which showed that an oncogenic enzyme inhibited Bcl-xL deamidation, promoted Bcl-xL–Bim binding, and allowed DNA-damaged developing T cells (called thymocytes) to survive in a mouse model of T cell lymphoma—the researchers concluded that Bcl-xL deamidation is a “critical switch” in transforming T cells. This evidence concerns the gene BCL2L1 and T-cell non-Hodgkin lymphoma.