Recently, the junctional adhesion molecule-A (JAM-A) has emerged as a crucial mediator between MM plasma and medullary endothelial cells, and has been associated with poor prognosis of MM patients due to its role in invasion and metastasis [105,106]; while limited so far, evidence suggests that JAM-A could also interfere with the VEGF/VEGFR pathway [107]. This evidence concerns the gene F11R and Miyoshi myopathy.