Together with the fact that CXCR4-CXCL12 signaling activates several pathways like Janus kinases-signal transducer and activator of transcription (JAK-STAT), phosphoinositide 3-kinase (PI3K), protein kinase B (PKB, AKT), mitogen-activated protein kinase (MAPK), and NF-κB [43,44,45], we hypothesize that the high co-occurrence of the receptor and its ligand influences the resistance of lymphomas toward anti-lymphoma therapy. This evidence concerns the gene CXCR4 and lymphoma.