The similarities in the epigenetic mechanism of regulation between cDLBCL and other human cancers, as well as evidence of antitumourigenic activity of CiDEA, MAL and PCDH17 after ectopic re-expression in other human cancers, led us to hypothesise that these three genes, whose expression was restored by epigenetic drugs, could represent new potential drivers in cDLBCL. Here, MAL is linked to cancer.