Consistent with this hypothesis, transgenic mice over‐expressing MYC along with either RUNX1 or RUNX2 display rapid onset of T or B‐cell lymphomas.5, 6 Furthermore, retroviral mutagenesis screens in CD2‐RUNX2 mice identified both MYC and MYCN as preferred targets for activation, indicating a strong selection for co‐activation of both gene families as drivers of lymphoma.7 The gene discussed is RUNX2; the disease is B-cell non-Hodgkin lymphoma.