RUNX2 and Miyoshi myopathy: MSCs derived from patients with MM had abundant exosomal lncRNA RUNX2-AS1; further studies revealed that it could be transferred from MM cells to MSCs and thereby prevent MSC osteogenesis by downregulating RUNX2 (Li B. et al., 2018), which provides a novel pathological mechanism of the bone lesion in patients with MM and could be a potential therapeutic target in the future.