IL-17A produced by activated Th17 cells induced a semi-mature phenotype of CD14+ DCs with expressing NF-κB, CD68, CD1a, MHC II and CCR6 and induced cell fusion.80 IL17A-transdifferentiated iDCs in MM patients showed increased transcription of OCs-maturation genes (i.e., NFATC1 and FOS), which was explainable for the progressive bone destruction.138 Taken together, these studies emphasized the involvement of RANKL+ T cells under inflammatory conditions and IL-17-producing Th17 cells in DCs-derived osteoclastogenesis. Here, IL17A is linked to Miyoshi myopathy.