Nonetheless, many PRDMs are involved in cancer initiation and/or maintenance, such as (i) PRDM1, a tumor suppressor in diffuse large B cell lymphoma (DLBCL) and other hematological tumors [15,16]; (ii) PRDM2, which is frequently deleted or rearranged in multiple cancer types; (iii) PRDM5, which is frequently silenced in multiple types of cancer [17]; (iv) PRDM14, a unique epigenetic regulator, upregulated in nearly 25% of human lymphoid neoplasms [18]; and (v) PRDM15, which we have observed to be overexpressed in human lymphomas [19,20,21]. This evidence concerns the gene PRDM14 and diffuse large B-cell lymphoma.