The pathogenic importance in CLL of B‐cell receptor (BCR)‐ and toll‐like receptor (TLR)‐signals that employ BTK is emphasized by the remarkable activity of ibrutinib.1, 3 Growth and survival of CLL cells are also affected by cytokines that signal through ibrutinib‐insensitive janus kinases (JAKs).4, 5 Plasma levels of many cytokines are reduced by ibrutinib in CLL patients but IL4, IL6, and others are not changed significantly,6 could continue to support CLL cells, and lead ultimately to disease progression. This evidence concerns the gene IL4 and B-cell chronic lymphocytic leukemia.