It has been recently suggested that p53‐defective CLL cells are less dependent on BCR‐signaling34 and we have shown that CLL cells with 17p deletions have exaggerated responses to cytokines like type 1 interferons.35 Perhaps the presence of a 17p deletion or p53 mutation is a biomarker for CLL cells that are more dependent on JAK‐signaling and consequently more responsive to the combination of ibrutinib and ruxolitinib. Here, BCR is linked to B-cell chronic lymphocytic leukemia.