In GCB DLBCL, PTEN deletions and amplification of the microRNA-17-92 cluster (MIR17HG) sustain cell proliferation [34], while similar deregulations are also in place in Burkitt lymphoma (BL) cells, in which the constitute activation of the MYC oncogene directly activates the PI3K/Akt/mTOR pathway [35,36]. This evidence concerns the gene AKT1 and Burkitt lymphoma.