We herein demonstrated that in CLL cells both JAK2 and STAT3 are over-expressed as compared to normal B lymphocytes, STAT3 is constitutively phosphorylated on Tyr705 in the majority of patients, and bone marrow-derived MSCs sustain CLL survival through the activation of JAK2/STAT3 signaling. The gene discussed is JAK2; the disease is B-cell chronic lymphocytic leukemia.