Recent data demonstrated that the molecular mechanism underlying DC abnormalities in CLL is a disruption of the IL-4R/STAT6 pathway due to enhanced levels of the suppressor of cytokine signaling 5 (SOCS5), a negative regulator that inhibits STAT6 activation and leads to a defective DC differentiation (72). The gene discussed is STAT6; the disease is B-cell chronic lymphocytic leukemia.