B-cell acute lymphoblastic leukemia (B-ALL) is the most common cancer in children, and there is growing evidence for the inherited basis of ALL susceptibility.1 The majority of leukemia risk genes identified thus far are involved in either lymphoid differentiation (e.g., ETV6, PAX5, IKZF1, and TCF3)1–5 or cell cycle and apoptosis signaling (e.g., CDKN2A and TP53).6,7 DNA damage repair has also been implicated in the pathogenesis of both lymphoid and myeloid leukemias. Here, TP53 is linked to acute lymphoblastic leukemia.