Taking in consideration these findings, we could hypothesize that PVR overexpression renders MM cells more susceptible to NK cell mediated attack at early stage of diseases, while leading to a defective NK cell activity during disease progression when receptor repertoire of these cytotoxic lymphocytes results altered and the interaction PVR/TIGIT or PVR/CD96 may play a dominant role in the BM MM microenvironment. The gene discussed is TIGIT; the disease is Miyoshi myopathy.