Previous studies in DLBCL have suggested that the mechanism is not via regulation of CIITA expression but rather through an unknown transcriptional regulator.24, 26 Certainly FOXP1 silencing in ABC-DLBCL can increase the transcription and cell-surface expression of molecules under the transcriptional control of the CIITA complex, such as HLA-DRA and CD74. This evidence concerns the gene HLA-DRA and diffuse large B-cell lymphoma.