Thus, as down-regulation of CTLA-4 expression results in the increase and phosphorylation of STAT1 in CLL cells [21] and CTLA-4 blockade may lead to an increased level of pp38MAPK [42], we cannot exclude that the increased proliferation activity in the high CTLA-4 expressors following CTLA-4 blockade might result from activation of STAT pathways. The gene discussed is STAT1; the disease is B-cell chronic lymphocytic leukemia.