Strikingly, there are no reports of RUNX2 point mutations in cancer and most biological associations between RUNX2 and cancers indicate gain-of-function effects, as is exemplified by over-expression of RUNX2 by protein stabilization or gene amplification in osteosarcoma [23-27] or ectopic induction by retroviral insertion in c-Myc related T cell lymphomas [32-35]. This evidence concerns the gene MYC and osteosarcoma.