Although the most robust way of capturing the contribution of MYC and BCL2 to DLBCL pathogenesis is to identify the translocations deregulating their expression, there is solid evidence that a clinically substantive increase in expression of MYC and BCL2 may depend on genetic and epigenetic events that occur in addition to translocations [20, 46]. The gene discussed is MYC; the disease is diffuse large B-cell lymphoma.