To answer this question, and to elucidate whether the Ca2+ buffering capacity of CR, or on the contrary, its Ca2+ sensor function is implicated in the proliferation/survival of MM cells, we overexpressed the CaBPs (I) PV, considered as a “pure” Ca2+ buffer (II) CB, a Ca2+ buffer protein with reported Ca2+ sensor functions, and (III) CR in different MM cell lines with various endogenous CR expression levels and performed a set of “rescue experiments” by downregulating CR expression via a lentiviral approach. The gene discussed is CALB2; the disease is Miyoshi myopathy.