As with MYC, BCL2 can be deregulated through various mechanisms that include (i) indirect ones, such as the activation of signaling pathways [e.g., Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/AKT) or Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB)] and loss of Myeloid Leukemia 1 (MCL-1), and (ii) direct lesions, such as somatic mutations (restricted to FL with increased risk of transformation to DLBCL), amplifications, hypomethylation of the gene promoter or translocations with immunoglobulins[25]. This evidence concerns the gene MYC and diffuse large B-cell lymphoma.