Later on, additional studies confirmed the biological role of miR-29b in the context of the BMM; in detail, miR-29b overexpression impaired MM and HUVEC migration and increased adhesion to BMSCs, downmodulating the expression of factors involved in both angiogenesis and disease progression as IL-8, MMP2, and VEGF-A [102]. The gene discussed is VEGFA; the disease is Miyoshi myopathy.