Considering the substantial ongoing effort to optimize NK cell-based immunotherapies supported by the promising anti-MM activity of expanded activated NK cells [29, 30], in this work we aimed to understand: i) if BM NK cell infiltration can be affected by changes of homing receptor expression and function occurring upon in vitro activation; ii) if inhibition of CXCR3 on NK cells could increase the efficacy of NK cell-based adoptive immunotherapy strategies. The gene discussed is CXCR3; the disease is Miyoshi myopathy.