Previous studies have validated the connection between AGO2 and early disease-related death in MM patients [34], and AGO2 silencing has been shown to inhibit cell viability in MM cell lines through decreased miR-106a, miR-106b, miR-17-5p and miR-20b expression and consequent further activation of the cyclin-dependent kinase inhibitors p21Waf1/Cip1 and p27Kip1 [29]. This evidence concerns the gene CDKN1B and Miyoshi myopathy.