,53,54 It is possible that the aforementioned functions of MYC could synergize with the effects of a “second hit” (BCL-2 overexpression and/or TP53 mutation) affecting sensitivity to RiBi inhibition, thus contributing to determine the clinical aggressiveness and chemoresistant phenotypes observed in MYC/BCL-2 double-expresser lymphoma. The gene discussed is TP53; the disease is lymphoma.