An in vitro study of AML showed that abrogation of CD200-CD200R interaction enhances the T cell-stimulatory capacity of DCs [100], whereas inhibition of CD200-CD200R interaction was already investigated in clinical trial phase I/II in patients with relapsing or refractory B cell chronic lymphocytic leukemia or multiple myeloma. This evidence concerns the gene CD200R1 and AL amyloidosis.