Based on total H3K79 methylation levels we did not observe crosstalk between HDAC and DOT1L in the context of CTCL cells treated with the pan-HDAC inhibitor Vorinostat, i.e. treatment of CTCL cells did not lead to an increase in H3K79me or H3K79me2. This evidence concerns the gene DOT1L and primary cutaneous T-cell non-Hodgkin lymphoma.