Given the pleiotropic pro‐survival functions of PIMs, their increased expression in the lymph node‐resident CLL cells will likely facilitate drug resistance, increase metabolic fitness and protect CLL cells from proapoptotic stimuli.38, 39 Accordingly, inhibition of PIMs in CLL cells with SEL24‐B489 decreased phosphorylation of PIM substrates (p‐FOXO1, p‐4EBP1 and p‐BAD) and exhibited direct proapoptotic activity, regardless of the support from stromal cells. Here, BAD is linked to B-cell chronic lymphocytic leukemia.