As early divergers from other eukaryotes, kinetoplastids have several unusual features of gene regulation. For example, genes are post-transcriptionally processed from polycistronic transcription units and contain a hypermodified base, base J (β-D-glucosyl-hydroxymethyluracil), that demarcates the sites of transcription initiation and termination. In Leishmania spp., the loss of base J results in genome-wide defects in the termination of transcription, but only a partial defect is observed in Trypanosoma brucei. Two new studies now establish that the histone mark H3.V is required in addition to base J to terminate transcription by RNA polymerase II in T. brucei. Furthermore, the studies found that H3.V, but not base J, mediates the termination of transcription by RNA polymerase I at telomeric loci that encode variant surface glycoproteins. Therefore, H3.V may contribute to the antigen switching that occurs at these loci, which hides T. brucei from the host immune system.