In particular, it has been shown that monoclonal antibodies and small glycomimetic molecules (GMI-1070) that block the interactions between the MM cells and P-selectin reverse the microenvironment-induced in vitro and in vivo resistance to bortezomib, identifying P-selectin as a possible new therapeutic target in MM [23,29]. The gene discussed is SELP; the disease is Miyoshi myopathy.