However, more recent in vivo studies based on the combination of four MCD-DLBCL-associated hallmark genetic aberrations (Myd88L265P, Cd79B, and Prdm1 mutations, with or without BCL2 amplification) revealed a different phenotype from that of Tbl1xr1-deficient mice, questioning a memory B-cell origin for this DLBCL molecular subtype [94]. This evidence concerns the gene BCL2 and diffuse large B-cell lymphoma.