For instance, Zhang et al. [30] reported that MM cells released splicing factor arginine/serine-rich 8 (SFRS8) through exosomes to stimulate OCs’ malignant differentiation via facilitating the alternative splicing of the calcyclin-binding protein (CACYBP) independent of the Wnt/β-catenin pathway, meanwhile augmenting bone lesion formation in the SCID/NOD-TIBIA mouse model in vivo. The gene discussed is CACYBP; the disease is Miyoshi myopathy.