Considering the key role of CXCL12 in the localization of NK cells in BM, subversion of the CXCR4/CXCL12 axis has been hypothesized to represent a mechanism of immune evasion from NK-mediated immune surveillance in neuroblastoma and multiple myeloma (39, 55). This evidence concerns the gene CXCL12 and AL amyloidosis.