One such example is dependency of DLBCL on SIRT3 that can be suppressed using mitochondrial‐targeted class I sirtuin inhibitors.126 BL develops dependency on BCR‐dependent GSK3 inhibition and evolve mechanisms to bypass BCR loss such as RAS mutations.127 Combination therapies that target both BCR‐positive and ‐negative tumor cells may therefore show better efficiency. This evidence concerns the gene SIRT3 and diffuse large B-cell lymphoma.