We previously demonstrated that the PTR1 domain of HAPLN1 (HAPLN1-PTR1), produced as recombinant glutathione-S-transferase (GST) fusion (GST-PTR1), induces pro-survival NF-κB signaling in a manner resistant to the PI bortezomib and confers resistance to this clinical drug in several human MM cell lines tested relative to GST negative control [31]. This evidence concerns the gene HAPLN1 and Miyoshi myopathy.