The oncogenic potential of RUNX2 was first discovered through its identification as a target for transcriptional activation in a retroviral mutagenesis screen in transgenic mice overexpressing MYC in the T‐cell compartment (CD2‐MYC).1 It was subsequently shown that any of the three murine Runx family genes can be selected for activation in this transgenic model,2, 3, 4 suggesting a redundant oncogenic role for RUNX overexpression in the context of MYC‐induced lymphoma. This evidence concerns the gene MYC and lymphoma.