We were able to demonstrate that, in parallel to disease progression from MGUS to MM and plasma cell leukemia, the number of monocytic MDSCs appears to increase and they may express more IL-4R, which is critical for suppression of MDSC function through the L4Ra-STAT6 pathway and thereby indicative of greater immune-related activity [32]. The gene discussed is STAT6; the disease is Miyoshi myopathy.