Since the PI3K/Akt signaling pathway is central to CXCR4 signaling [51], plerixafor could possibly attenuate the translocation-induced deregulation of MYC and BCL2. In agreement, Chen et al. observed an association between CXCR4-positivity of DLBCL tumor samples and high expression of MYC as well as BCL2 [19]; whereas Hatano et al [60] demonstrated decreased c-Myc expression and Mao et al. [61] decreased Bcl-2 expression upon plerixafor administration, though in prostate cancer cells and brain tissue, respectively. This evidence concerns the gene BCL2 and neoplasm.