A Th2 phenotype might be protective against ALL development [119], while pro-inflammatory Th1 cells with high interferon gamma (IFNγ) levels have been shown to migrate towards BCP-ALL cells and favor their proliferation via upregulation of CD38 and IFNγ-induced protein 10 (IP-10) production [120••] mediated by activation-induced cytidine deaminase (AID) upregulation [121]. This evidence concerns the gene CXCL10 and acute lymphoblastic leukemia.