More recently, our observations in a mouse model of multiple myeloma led us to hypothesize that increased expression of CXCR3 ligands in the tumor BM microenvironment constitutes a new mechanism to avoid tumor infiltration by NK cells: ligand-induced CXCR3 activation on KLRG1− NK cells resulted in cross-desensitization of CXCR4 that together with the coincident down-modulation of CXCL12 protein levels promotes NK cell egress from BM into blood circulation. The gene discussed is CXCR3; the disease is AL amyloidosis.