Given the poor prognosis of these DLBCL subsets, the well-established oncogenic cooperation between MYC and BCL-2, and the known role of BCL-2 in oxidative stress response, these data are in line with a model whereby BCL-2 overexpression and constitutive DDR activation could provide a tolerance mechanism to MYC-induced replicative and oxidative stress. The gene discussed is MYC; the disease is diffuse large B-cell lymphoma.