Moreover, synthetically engineered DLBCL models, generated immediately by the directed mutations in human cell lines, or by their combination with mice of a specific genetic background, have enabled co-operating genetic alterations to be studied [46,48], such as FOXP1 silencing, BCR pathway expression or silencing, the co-expression of BCL2/MYC or BCL2/BCL6, and the expression of GC-DLBCL or ABC-DLBCL-related genes [29,49,50]. The gene discussed is MYC; the disease is diffuse large B-cell lymphoma.