Focusing on cluster’s molecular function, antagomirs-mediated inhibition of miR-221/222 resulted in reduced cell proliferation through the upregulation of the p27Kip1 and p57Kip2 cyclin-dependent kinase inhibitors (CDKIs), while overexpression of the cluster triggered p27Kip1 downregulation and subsequently promoted S-phase, highlighting the potential impact of miR-221/222-p27Kip1/p57Kip2 axis in cell-cycle regulation of MM plasma cells [37]. The gene discussed is CDKN1C; the disease is Miyoshi myopathy.