The significant correlation between the extent of VLA-4 positivity of the sample and the BM homing capacity of the cells is in line with our previous observation of reduced circulation capacity of CLL cells at early Rai stages, which displayed lower VLA-4 expression than normal B lymphocytes.[12] More importantly, clinically, the VLA-4 state is directly manifested in the extent of human BM infiltration while the CD38 state did not influence it (Fig. 4A). This evidence concerns the gene CD38 and B-cell chronic lymphocytic leukemia.