In the frame of tumor immunotherapy, previous indications that the introduction of GFP at the N‐terminal part of Foxp3 affects its interaction with HIF1‐alpha and IRF4 9, HDAC7, Tip60 and Eos 10, or PRC2 12 open the possibility that identification of peptides interfering specifically with either of these interactions could provide novel therapeutic tools, as is already developed for Foxp3 C‐terminal part‐NFAT interactions 24. The gene discussed is IRF4; the disease is neoplasm.