Although PIM isoforms are highly homologous and share an overlapping spectrum of substrates, in CLL cells they exhibit non‐overlapping, yet highly complementary functions, whereby PIM1 is essential for CXCR4‐dependent CLL cell migration and PIM2/3 for cell survival.9, 15, 46 Thus, inhibition of all PIM isoforms is a rational approach, excluding possibility of isoform redundancy or compensation issues. This evidence concerns the gene CXCR4 and B-cell chronic lymphocytic leukemia.