In line with our research, a study by Ramírez-Salazar et al. [50] demonstrated that the targets of the down-regulated hsa-miR-101-3p in MM were significantly enriched in pathways in cancer, including the signaling molecule mitogen-activated protein kinase 1 (MAPK1), the transcription factor v-ets erythroblastosis virus E26 oncogene homolog 1 (ETS1), and the mesenchymal transition-associated molecule frizzled class receptor 4 (FZD4). The gene discussed is ETS1; the disease is Miyoshi myopathy.