Despite we found an increase of several components of the IL17 signaling (IL17RA, TRAF6, TYK2) and its downstream effectors CEBPD and CEBPB in both MM and MGUS HDNs, we did not test in vitro the effect of IL17 on neutrophils function, because of lack of ILR17C, required for the full receptor assembly to work properly81,82. The gene discussed is TRAF6; the disease is Miyoshi myopathy.