p53 signalling in TKI-naïve CML CD34+ cells is indeed lower than that found in normal CD34+ cells18, suggesting LSC self-renewal may be more sensitive to levels of p53 activity than that of HSC, and lowering p53 levels in LSC may be required to balance out the proliferative effects of BCR::ABL1. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.