The CD200 blockade improved the regulation of AML growth by Tr1cells engineered to overexpress IL-10 [42], a phenomenon reminiscent of a claim that Ibrutinib, an inhibitor of Bruton’s tyrosine kinase (BTK) and IL-2-inducible T cell kinase (ITK), which is used in the treatment of CLL, alters CD200 expression and thus CLL-induced immunosuppression [43]. This evidence concerns the gene CD200 and acute myeloid leukemia.